Pubmed abstracts for Protein-Protein Interaction search result :

Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Analysis of the activation of the proto oncogene , akt , demonstrates a possible link of the p70S6K activating pathway to carcinogenesis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We therefore examined the role of PI ( 3 ) K , its upstream effector Ras , and its putative downstream protein kinase effectors PKB / Akt and p70S6K ( ref . 5 ) in the modulation of apoptosis induced in fibroblasts by the oncoprotein c Myc . ^^^ Here we show that Ras activation of PI ( 3 ) K suppresses c Myc induced apoptosis through the activation of PKB / Akt but not p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The fact that PKC zeta stimulates general protein synthesis but not activation of p70S6K indicates that PKC zeta activation does not involve the proto oncogene Akt , which is also activated by PI3K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These data indicate that the activation of p 70 S6k by arsenite involves p 38 MAP kinase and phosphatidylinositol 3 kinase but not PKB . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These results indicate a bifurcation or subcompartmentalization of the insulin signalling pathway whereby some targets of PI 3 K ( i . e . , p70s6k ) are dependent on IRS 1 associated PI 3 K and other targets ( i . e . , AKT and glucose transport ) are not . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Ser 222 , Ser 364 , and Ser 381 are situated in analogous positions to phosphorylation sites in protein kinase B , protein kinase C , and p70S6K , suggesting a common mechanism of activation for these growth factor stimulated protein kinases . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Differential regulation by calcium reveals distinct signaling requirements for the activation of Akt and p70S6k . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
A regulatory link between p70s6k and PKB was demonstrated , as PDK 1 was found to selectively phosphorylate p70s6k at Thr 229 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We provide evidence that apoptosis induced by triggering the CD 95 cell death receptor is counteracted by PI 3 kinase activation ; moreover , PKB but not p70S6K represents the relevant downstream target of PI 3 kinase signaling . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Here , we report that of five SCLC cell lines tested , all exhibited high basal constitutive phosphoinositide 3 kinase ( PI 3 kinase ) activity , which results in high basal protein kinase B ( PKB ) and ribosomal p 70 S6 kinase activity ( p70s6k ) . ^^^ The presence of a constitutively active phosphoinositide 3 kinase in small cell lung cancer cells mediates anchorage independent proliferation via a protein kinase B and p70s6k dependent pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Mixed hindlimb skeletal muscle lysates were used to determine the expression and enzymatic activities of the extracellular regulated kinase 2 ( ERK 2 ) , p 90 ribosomal S 6 kinase ( RSK 2 ) , Akt , and p 70 S6 kinase ( p70S6k ) . ^^^ In all three groups of rats , insulin significantly increased ERK 2 , RSK 2 , Akt , and p70S6k activities . ^^^ Islet transplantation partially ( RSK 2 ) or fully ( Akt , p70S6k ) normalized these diabetes induced changes in insulin signaling proteins . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In cells where cAMP is a mitogen , cAMP elevating agents stimulate membrane ruffling , Akt phosphorylation , and p 70 ribosomal S 6 protein kinase ( p70s6k ) activity . cAMP effects on ruffle formation and Akt were PKA independent but sensitive to wortmannin . ^^^ In contrast , cAMP stimulated p70s6k activity was repressed by PKA inhibitors but not by wortmannin or microinjection of the N terminal SH 2 domain of the p 85 regulatory subunit of PI3K , indicating that p70s6k and Akt can be regulated independently . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Recent studies have shown that Akt may play an intermediate role between phosphatidylinositol 3 kinase ( PI3K ) and p 70 S6 kinase ( p70S6K ) . ^^^ Here we show that a novel nuclear p70S6K related kinase ( SRK ) exists and that its in vivo function is also augmented by over expression of Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Overexpression of wild type Akt 1 promoted insulin stimulated p70S6 kinase ( p70S6K ) activity and affected GSK 3 beta regulation , but did not promote insulin stimulated GLUT 4 translocation or glucose transport in L 6 myotubes . ^^^ We found that overexpression of WT Akt 1 promoted insulin stimulated p70S6 kinase ( p70S6K ) activity and increased the basal activity of GSK 3 beta , but did not promote insulin stimulated GLUT 4 translocation or glucose uptake . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin also activated protein kinase B ( PKB ) , which may lie upstream of p 70 S6k and 4E BP 1 , with the activation of the different isoforms being in the order alpha > beta > gamma . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The inhibitory effects of the overexpressed JM domain were accompanied by inhibition of insulin stimulated IRS 1 phosphorylation , decreased IRS 1 associated PI3K activity , and decreased phosphorylation of the downstream effectors of PI3K , PKB and p 70 S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Inhibition of the downstream effectors of Rac , phosphatidylinositol 3 kinase ( PI 3 K ) and p70S6k , which are known to be constitutively activated by PyMT transformation , inhibited bEND . 3 cell proliferation and cyst formation in fibrin gels even in cells expressing V 12 constitutively active Rac , but they did not restore capillary tube formation . ^^^ The downstream Rac effectors , P 13 K and p70S6k , mediate PyMT / Rac effects on cell proliferation and cyst formation , but other unknown effectors of PyMT are required for the cytoskeletal changes and activation of the PA / plasmin system . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , AKT , but not protein kinase C zeta , is used by SCF / c kit / PI3 K to activate p70S6K . ^^^ Dominant negative AKT K179M completely abolished p70S6K phosphorylation induced by the constitutively active PI 3 K catalytic subunit p 110 . ^^^ Constitutively active 5 AKT highly phosphorylated p70S6K , which was totally inhibited by rapamycin . ^^^ Thus , SCF / c kit uses a rapamycin sensitive PI 3 K / AKT / p70S6K / cyclin D 3 pathway to promote spermatogonial cell proliferation . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In addition , Akt , the upstream component of p70S6k , was activated by zinc in a biphasic manner , as was p70S6k . ^^^ Moreover , dominant interfering alleles of Akt and PDK 1 blocked the zinc induced activation of p70S6k , whereas the lipid kinase activity of PI3K was potently activated by zinc . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The paradigm of Akt activation via phosphoinositide dependent phosphorylation provided a framework for research into the mechanism of activation of other members of the AGC kinase group ( p70S6K , PKC , and PKA ) and members of the Tec tyrosine kinase family ( TecI , TecII , Btk / Atk , Itk / Tsk / Emt , Txk / Rlk , and Bm / Etk ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Transient transfection assays with mTOR mutants bearing Ala substitutions at Ser 2448 and / or Thr 2446 indicated that AKT dependent mTOR phosphorylation was not essential for either PHAS 1 phosphorylation or p70S6K activation in HEK cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Although we found that EGF stimulated p70s6K phosphorylates through a MAPK dependent and a MAPK independent ( wortmannin sensitive ) pathway , TGF beta 1 failed to block EGF triggered phosphorylation of p70s6K at thr ( 389 ) and thr ( 421 ) / ser ( 424 ) sites , implying that PKB inhibition by TGF beta 1 may result from inhibition of PDK 1 activity instead of inhibition of PI3K activity . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Despite the expression of PTEN with the concomitant low Akt activity in all mouse PCT lines , their p70S6K activities were generally higher than those in 3 human MM lines , arguing for specific negative regulation of Akt , but not p70S6K by PTEN . ^^^ These results suggest that p70S6K and Akt may be differentially used by the plasma cell tumors derived from mice and humans , respectively . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt activation was blocked by inhibitors of phosphatidylinositol 3 kinase , but not by an inhibitor of the ribosomal protein kinase p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Vanadate treatment also led to the increase of active MEK , increased phosphorylation of p70s6K at thr 389 , thr 421 , and ser 424 yet without activation of PKB . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Over expression of constitutively active forms of Akt promotes cell proliferation and survival , and also stimulates p 70 S6 kinase ( p70S6K ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Analysis of several elements of signaling pathways which are known to regulate protein synthesis in a positive manner ( p42 / p44 MAPK , AKT and p 70 S6K stimulation , and hyperphosphorylation of PHAS 1 ) were not inhibited but rather were stimulated by orthovanadate . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of p70s6K , Akt , and cdc 2 was evaluated by Western blot . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The lipid kinase phosphoinositide 3 OH kinase ( PI ( 3 ) K ) and some of its downstream targets , such as the protein serine / threonine kinases Akt and p 70 S6 kinase ( p70S6K ) , are crucial effectors in oncogenic PTK signalling . ^^^ This review emphasizes how oncogenic conversion of protein kinases results from perturbation of the normal autoinhibitory constraints on kinase activity and provides an update on our knowledge about the role of deregulated PI ( 3 ) K / Akt and mammalian target of rapamycin / p70S6K signalling in human malignancies . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The cellular kinases Akt and p70S6K and the transcription factor NF kappaB were activated in a PI 3 K dependent manner at similar times following HCMV infection . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , they inhibited the PRL dependent stimulation of the SFKs substrate Sam 68 , the phosphorylation of the tyrosine phosphatase Shp 2 , and the PI3K dependent Akt and p70S6k serine kinases . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Whereas insulin gene transcription is promoted by signaling through insulin receptor A type ( Ex 11 ) , PI3K class Ia , and p70s6k , insulin stimulates the betaGK gene by signaling via insulin receptor B type ( Ex11+ ) , PI3K class 2 like activity , and PKB ( c Akt ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
BAPTA AM pretreatment inhibited other insulin induced phosphorylation events including phosphorylation of Akt , MAPK ( ERK 1 and 2 ) and p 70 S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These changes were observed in the absence of an activation of either protein kinase B ( PKB , akt 1 ) or p 70 S6 kinase ( p 70 S6K ) . ^^^ It may be concluded that aberrant mitogenic signaling in human breast cancer in vivo involves Pak , p 38 MAPK and MAPKAPK 2 downstream of PI 3 K , but neither of PKB or p 70 S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
It also activated Akt and p70S6 kinase ( p70S6K ) but not p 38 MAPK . ^^^ By contrast , LY 294002 inhibited HB EGF induced Akt and p70S6K activation without effecting ERK activation by HB EGF . ^^^ These results demonstrate that HB EGF induced mitogenesis requires both ERK and phosphatidylinositol 3 kinase ( Akt and p70S6K ) pathways activated through EGFR , thereby providing a new mechanistic insight by which HB EGF contributes to vascular remodeling . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The PI 3 K pathway was examined by following phosphorylation ( activation ) of two of its downstream kinases , Akt and p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The phosphorylation of two downstream effectors of phosphoinositide 3 kinase , Akt and p70S6K , was markedly inhibited in the presence of artesunate . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt , an upstream kinase of p70S6K , was also deactivated by 2 days of treatment of DSG . ^^^ These results demonstrate that DSG inhibits tumor cell growth through the inhibition of protein synthesis and induction of apoptosis , which is caused by the down regulation of Akt kinase and p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin restores differentiation of Ras transformed C2C12 myoblasts by inducing NF kappaB through an AKT / P70S6K / p38 MAPK pathway . 5 H ras transformed C2C12 ( C2Ras ) myoblasts , overexpressing p 21 Ras protein in the Ras GTP active form , showed a differentiation defective phenotype when cultured in low serum as compared with C2C12 myoblasts . ^^^ Inhibition of p42 / p44 MAPK with the chemical inhibitor PD 98059 , and activation of AKT / P70S6K and p 38 MAPK with insulin , produced growth arrest ( precluding the expression of PCNA , cyclin D 1 and retinoblastoma at the hyperphosphorylated state and inducing the expression of the cell cycle inhibitor p 21 ( Cip ) ) and myogenesis ( multinucleated myotubes formation and induction of creatine kinase , caveolin 3 and alpha actin ) . ^^^ Finally , transient transfection of a constitutively active Myr EGFP AKT HA construct ( in the presence of PD 98059 ) restored C2Ras myogenesis by its ability to activate P70S6K and p 38 MAPK . ^^^ A crosstalk between P70S6K and p 38 MAPK was observed under rapamycin treatment in both insulin or active AKT induced myogenesis . ^^^ Our results are delineating an AKT / P70S6K / p38 MAPK pathway involved in skeletal muscle differentiation . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
On the other hand , LY 294002 and wortmannin , specific inhibitors of PI3K , prevented PDGF BB induced phosphorylation of Akt and its downstream effector molecules , p70S6K , ribosomal protein S 6 , 4E BP 1 , and eIF4E . ^^^ NEM also abrogated the phosphorylation of p70S6K , ribosomal protein S 6 , 4E BP 1 , and eIF4E induced by PDGF BB , suggesting that thiol alkylation interferes with the PI3K / Akt pathway at the level of Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Differential effects of des IGF 1 on Erks , AKT 1 and P 70 S6K activation in mouse skeletal and cardiac muscle . ^^^ Alterations in the degree of the phosphorylation of ERKI / 2 , Akt 1 and p 70 S6K in mouse skeletal and cardiac muscle was examined in vivo following an intraperitoneal injection of des IGF 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In addition , 5 ( S ) HETE stimulated phosphatidylinositol 3 kinase ( PI 3 kinase ) activity and phosphorylation of its downstream targets Akt , p70S6K , and 4E BP 1 and their effector molecules ribosomal protein S 6 and eIF4E . ^^^ Interestingly , AG 490 attenuated 5 ( S ) HETE induced PI 3 kinase activity and phosphorylation of Akt , p70S6K , ribosomal protein S 6 , 4E BP 1 , and eIF4E . 5 ( S ) HETE induced the expression of basic fibroblast growth factor 2 ( bFGF 2 ) in a Jak 2 and PI 3 kinase dependent manner . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
TSH activated p 70 S6K and protein kinase B ( PKB / Akt ) , as measured by immunoblot analysis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In this study the authors evaluated whether the phosphatidylinositol 3 kinase ( PI 3 K ) Akt p70S6K pathway is expressed in meningiomas , regulates their growth , and transduces mitogenic signals of PDGF BB . ^^^ METHODS : Nine meningioma tumors obtained in humans were evaluated using Western blot analysis for phosphorylated ( activated ) Akt and phosphorylated p70S6K . ^^^ Cells cultured from seven of these meningiomas were also screened using Western blot analysis for Akt and for phosphorylated Akt and p70S6K . ^^^ The authors also evaluated whether PDGF BB stimulation of meningioma cells was associated with the phosphorylation of Akt and p70S6K known to activate these kinases . ^^^ In addition , the effects of wortmannin , an inhibitor of P 13 K , on proliferation and activation of Akt and p70S6K in meningioma cells stimulated with PDGF BB were evaluated . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
On growth factor stimulation , tuberin , the TSC 2 protein , is phosphorylated by Akt , thereby releasing its inhibitory effects on p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , the inhibitory effects of wortmannin are markedly accentuated in cells overexpressing PKB or p70S6K ( CHO ( PKB ) and CHO ( p70S6K ) cells ) , whose adhesion and spreading on galectin 8 ( but not on fibronectin ) is inhibited approximately 25 35 % in the presence of wortmannin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of Akt , p70S6k , and signal transducer and activator of transcription 3 ( STAT 3 ) peaked on recovery day 3 compared with day 0 . ^^^ In addition , transient peaks in seven protein concentrations occurred at different times of recovery : STAT 3 , calcineurin A ( CaNA ) , CaNB , and beta4E BP 1 protein concentrations peaked on the third recovery day ; p70S6k , STAT 3 , Akt , and GSK 3 beta peaked on the sixth recovery day ; and GSK 3 beta peaked on the fifteenth recovery day . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Both p70S6 kinase ( p70S6K ) and Akt are kinases downstream of phosphatidylinositol 3 kinase ( PI3K ) . ^^^ Tumorous and adjacent normal tissues of 20 patients with papillary thyroid cancer were obtained at surgery , and expression of p70S6K and Akt were measured by Western blot . ^^^ The data presented here demonstrate that both p70S6K and Akt are activated in the majority of human papillary cancer cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt expression led to p70S6K activation , prostatic intraepithelial neoplasia ( PIN ) , and bladder obstruction . mRNA expression profiles from MPAKT ventral prostate revealed similarities to human cancer and an angiogenic signature that included three angiogenin family members , one of which was found elevated in the plasma of men with prostate cancer . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Age related differences in the des IGF 1 mediated activation of Akt 1 and p 70 S6K in mouse skeletal muscle . ^^^ The ability of des IGF 1 to activate Akt 1 and p 70 S6K in skeletal muscle with or without acute endurance exercise was examined in young and old mice . ^^^ Blood and skeletal muscle were collected and IGF 1 receptor , Akt 1 and p 70 S6K protein contents and their phosphorylation status were determined . ^^^ Des IGF 1 mediated Akt 1 and p 70 S6K phosphorylation was not changed by exercise in either young or old mice . ^^^ It is concluded that there was an aging related resistance at the p 70 S6K level in mouse skeletal muscle that could not be restored by prior exercise and this resistance is associated with lower IGF 1 receptor number and Akt 1 phosphorylation in the aged skeletal muscle . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The Src inhibitor PP 1 abrogated PRL dependent in vivo activation of Fak , Erk1 / 2 , p70S6K , and Akt and the proliferation of T47D and MCF 7 cells ; Janus kinase 2 ( Jak 2 ) activation was not affected . ^^^ Expression of Fak mutant Y397F abrogated PRL dependent activation of Fak , Erk1 / 2 , and thymidine incorporation , but had no effect on p70S6K and Akt kinases . ^^^ MAPK kinase 1 / 2 ( Mek1 / 2 ) inhibitor PD 184352 blocked PRL induced stimulation of Erk1 / 2 and cell proliferation ; however , p70S6K and Akt activation were unaffected . ^^^ The phosphatidylinositol 3 kinase ( PI3K ) inhibitor LY 294002 abolished cell proliferation and activation of p70S6K and Akt ; however , PRL dependent activation of Erk1 / 2 was not modified . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
GDNF induces the phosphorylation of Akt and p70S6 kinase ( p70S6K ) in SH SY5Y cells in which Ret protein expression is relatively low . ^^^ Interestingly , treating SH SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF induced Ret tyrosine phosphorylation , but does not affect the mitogenic action of GDNF and the activation of the Akt / p70S6K pathway . ^^^ These results suggest that GDNF promotes cell proliferation via the activation of p70S6K , independent of the ERK signaling pathway , and that GDNF activates the Akt / p70S6K pathway more efficiently than the ERK pathway in the cells in which Ret expression is low . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Treatment with rapamycin inhibited EGF induced phosphorylation and activation of ribosomal p 70 S6 protein kinase ( p 70 S6K ) , an mTOR downstream target , but had no effect on phosphorylation and activation of Akt . ^^^ The expression of DNM Akt 1 also suppressed EGF induced p 70 S6K activation as well as Akt activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The addition of insulin induced rapid activations of p70S6K and Akt , and the cells were rescued from macroautophagy . ^^^ Low doses of LY 294002 , a phosphatidyl inositol 3 kinase inhibitor , which abolished cell growth and p70S6K activity but did not influence Akt activity , did not block the insulin mediated rescue either . ^^^ By contrast , low doses of Akt specific inhibitors , which inhibited neither cell growth nor p70S6K activity , completely blocked the insulin mediated rescue from macroautophagy . ^^^ Thus , insulin dependent signals are responsible for the control of azurophil granule selective macroautophagy via Akt dependent pathways , while p70S6K dependent pathways promote cell growth . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We hypothesized that PI3K / PDK1 / Akt / mTOR / p70S6K mediated pro survival pathway is involved in delayed cardioprotection induced by IPC . ^^^ Western blot analysis showed that wortmannin , at a dose of 0 . 6 mg / kg , and rapamycin , at a dose of 0 . 25 mg / kg , were sufficient to prevent phosphorylation of Akt and p70S6K , respectively , when the inhibitors were given prior to IPC . ^^^ We conclude that PI3K / PDK1 / Akt / mTOR / p70S6K signalling pathway plays an essential role in the development of the cardioprotection against infarction in rabbits . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
At variance with Ly 294002 , the Akt inhibitor did not negatively affect phosphorylation of protein kinase C zeta and it was less effective in downregulating p70S6 kinase ( p70S6K ) activity . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Increased PDK 1 and phosphorylation of the 85 kDa regulatory subunit of PI 3 kinase , Akt and p70s6k were also observed . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Muscles of transgenic mice exhibited increased site specific phosphorylation on both Akt and p 70 ribosomal S 6 kinase ( p70S6k ) ( P < 0 . 05 ) before ablation , perhaps accounting for the enhanced response to synergist ablation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
However , in the early phase of apoptosis , ActD induced an increase in PLD activity and activation of key factors in the cell survival signalling pathways , such as PI3K ( phosphoinositide 3 kinase ) , Akt , p70S6K ( p 70 S6 kinase ) and ERK ( extracellular signal regulated kinase ) . ^^^ The PI3K inhibitor LY 294002 inhibited the ActD induced activation of Akt and p70S6K , and completely abolished the effects of PLD 1 or PLD 2 , whereas inhibition of ERK activity by the MEK inhibitor U 0126 had a milder effect . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These events were accompanied by the caspase independent downregulation of Raf 1 , inactivation of MEK1 / 2 , ERK , Akt , p70S6K , dephosphorylation of GSK 3 , and activation of c Jun N terminal kinase ( JNK ) and p 38 MAPK . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Moreover , stimulation of hypertrophy with growth hormone insulin like growth factor 1 ( GH IGF 1 ) failed to activate calcineurin NFAT signaling in the heart or in culture , despite hypertrophy , activation of Akt , and activation of p 70 S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin treatment induced p70S6K , mTOR , and Akt phosphorylation , effects that were completely prevented by the PI3K inhibitor , LY 294002 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This treatment also increased PI 3 kinase activation , PDK 1 expression , Akt phosphorylation and p70s6k phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
As several kinase mediated signal transduction pathways have been implicated in the development of cardiac hypertrophy and failure , we examined the activities of the Erks , MEKs , Akt , GSK 3 beta , p70S6K , JNKs and p 38 under LVAD support as well as during single myocyte strain and whole heart stretch . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Mammalian target of rapamycin ( mTOR ) is a PKB substrate , and regulates p 70 S6 kinase ( p 70 S6K ) . ^^^ Since p 70 S6K is an insulin responsive kinase downstream of PI3K and PKB , its potential role in adipogenic insulin signaling was investigated . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Activation of aPKC is required for vanadate induced phosphorylation of protein kinase B ( Akt ) , but not p70S6k in mouse epidermal JB 6 cells . ^^^ The present study investigated the vanadate induced phosphorylation of Akt and p70S6K , two kinases known to be vital for cell survival , growth , transformation , and transition of the cell cycle in mammals . ^^^ Exposure of mouse epidermal JB 6 cells to vanadium led to phosphorylation of Akt and p70S6K in a time and dose dependent manner . ^^^ Importantly , overexpression of a dominant negative mutant PKClambda blocked Akt phosphorylation at Ser 473 and Thr 308 , whereas it did not inhibit p70S6k phosphorylation at Thr 389 and Thr421 / Ser424 , suggesting that aPKC activation is specifically involved in vanadium induced activation of Akt , but not in activation of p70S6k . ^^^ Furthermore , vanadium induced p70S6k phosphorylation at Thr 389 and Thr421 / Ser424 and Akt phosphorylation at Thr 308 occurred through a PI 3K dependent pathway because a PI 3K dominant negative mutant inhibited induction as compared with vector control cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Unique , highly proliferative growth phenotype expressed by embryonic and neointimal smooth muscle cells is driven by constitutive Akt , mTOR , and p70S6K signaling and is actively repressed by PTEN . ^^^ Using immunohistochemistry and Western blot analysis , we report high levels of total and phospho S6RP and increased levels of Akt and p70S6K phosphorylation , upstream positive regulators of S6RP , in rat embryonic aortas and adult balloon injured carotid arteries compared with quiescent adult aortas and uninjured carotid arteries . ^^^ Western blot analysis demonstrated that cultured embryonic and neointimal SMCs that exhibited serum independent growth capabilities expressed high levels of S6RP and constitutively active Akt , mTOR , and p70S6K . ^^^ Growth of SMCs that exhibit this phenotype is dependent on constitutive Akt and mTOR / p70S6K signaling and is actively inhibited through the timed acquisition of the endogenously produced growth suppressor PTEN . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The induction of VEGF protein by Akt is associated with increased phosphorylation and thus activation of p70S6K and eIF4E binding protein 1 , leading to increased VEGF translation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We first explored the effect of GLP 1 , compared with that of insulin , on the activation of PI3K , PKB , p70s6 kinase ( p70s6k ) and p44 / 42 mitogen activated protein kinases ( MAPKs ) and the action of specific inhibitors of these kinases on the insulin and GLP 1 induced increment in glycogen synthase a activity . ^^^ The study showed that GLP 1 , like insulin , activated PI3K / PKB , p70s6k and p44 / 42 . ^^^ It was concluded that activation of PI3K / PKB and MAPKs is required for the GLP 1 induced increment in glycogen synthase a activity , while PKC , although apparently participating , does not seem to play an essential role ; unlike in insulin signaling , p70s6k , PP 1 and PP 2A do not seem to be needed in the action of GLP 1 upon glycogen synthase a activity in rat muscle . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In vivo phosphopeptide mapping revealed phosphopeptides common to those generated in vitro by AKT , p70S6K , MEK 1 , and MKK 6 , suggesting that these kinases may phosphorylate NS5A in mammalian cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
B [ a ] PDE exposure also led to activation of phosphotidylinositol 3 kinase ( PI 3K ) , Akt and p 70 S6 kinase ( p70S6k ) . ^^^ Furthermore , an overexpression of dominant negative Akt mutant , Akt T308A / S473A , blocked B [ a ] PDE induced activation of Akt , AP 1 and JNKs , while it did not affect the activation of p70S6k , ERKs and p 38 kinase . ^^^ These results demonstrated that B [ a ] PDE was able to induce AP 1 transactivation and this AP 1 induction was specific through PI 3K / Akt / JNKs dependent and p70S6k independent pathways . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The phosphatidylinositol 3 kinase ( PI3K ) inhibitors , wortmannin and LY 294002 [ 2 ( 4 morpholinyl ) 9 phenyl 4H 1 benzopyran 4 one ] , dominant negative Akt , or rapamycin , an inhibitor of mTOR ( mammalian target of rapamycin ) and ribosomal p 70 S6 kinase ( p70S6K ) phosphorylation , inhibited the insulin mediated increase in GCLC protein and GSH levels . ^^^ In conclusion , these data show that insulin signaling pathways involving PI3K / Akt / p70S6K , but not MAPKs , are active in the insulin mediated regulation of GSH synthesis via increased GCLC expression . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In response to IGF 1 , Akt activates downstream effectors , mTOR and p70S6K to stimulate protein synthesis thereby increasing the cytoplasmic compartment in muscle fibers . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
GPx 1 modulates Akt and P70S6K phosphorylation and Gadd 45 levels in MCF 7 cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
L 6 myoblast differentiation is modulated by Cdk 5 via the PI3K AKT p70S6K signaling pathway . ^^^ Here , we investigated whether PI3K , Akt , p70S6K , p 38 MAPK , p44 / 42 MAPK , and Egr 1 serve as upstream regulators of Cdk 5 during L 6 myoblast differentiation . ^^^ Upon serum reduction , we found that besides elevated expression of Cdk 5 and its activator , p 35 , and increased Cdk5 / p35 activity , Egr 1 , Akt , p70S6K , and p 38 MAPK activity were upregulated in differentiating L 6 cells . ^^^ LY 294002 , a PI3K inhibitor , blocked the activation of Akt and p70S6K , indicating that Akt and p70S6K activation is linked to PI3K activation . ^^^ Overexpression of dominant negative Akt also reduced Cdk5 / p35 activity and myogenin expression , indicating that the PI3K p70S6K Egr 1 Cdk 5 signaling cascade is linked to Akt activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In this study , EGF significantly stimulated HTR8 / SVneo cell migration and the phosphorylation of AKT , ERK1 / 2 and p70S6K in a concentration dependent manner . ^^^ In the presence of PI3K inhibitors ( Wortmannin ) , EGF stimulated trophoblast migration and phosphorylation of AKT and P70S6K ( Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) ) were decreased , while EGF induced ERK phosphorylation was not affected . ^^^ Expression of an activated AKT ( Myr AKT 2 ) increased basal phospho p70S6K ( Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) ) content , but failed to stimulate cell migration . ^^^ In addition , there was a concentration dependent inhibition of cell migration and p70S6K phosphorylation ( Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) ) in the presence of Rapamycin , a specific inhibitor of the mammalian target of rapamycin ( mTOR , a downstream of AKT ) . ^^^ Taken together , our data suggest that EGF induced trophoblast migration involves the coordinated regulation of both PI3K / AKT and MAPK signalling pathways . mTOR / p70S6K is important in PI3K but not MAPK mediated trophoblast migration in response to EGF . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Isolated perfused rat hearts were subjected to : ( a ) 35 minutes of ischemia and 120 minutes of reperfusion , and infarct size was determined by tetrazolium staining ; or ( b ) 35 minutes of ischemia and 7 minutes of reperfusion , and the phosphorylation states of Akt , endothelial NO synthase ( eNOS ) , and p70S6K were determined . ^^^ Western blot analysis demonstrated that Postcond induced a significant increase in phosphorylation of Akt , eNOS , and p70S6K in an LY and Wort sensitive manner . ^^^ In conclusion , we show for the first time that ischemic Postcond protects the myocardium by activating the prosurvival kinases PI3K Akt , eNOS , and p70S6K in accordance with the RISK pathway . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
TGF beta 1 modulates matrix metalloproteinase 13 expression in hepatic stellate cells by complex mechanisms involving p38MAPK , PI 3 kinase , AKT , and p70S6k . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
EGF induced phosphorylation of extracellular signal regulated kinases ( ERK ) 1 / 2 , c Jun N terminal kinase , p 38 , Akt , and p70S6K in BEAS 2B cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt activation was blocked by wortmannin and LY 294 , 002 , two inhibitors of PI 3 K ; by genistein , a protein tyrosine kinase inhibitor and an ER agonist ; by AG 825 , a selective ErbB 2 inhibitor ; and by the antiestrogens ICI 182 , 780 and 4 hydroxy tamoxifen ; but not by rapamycin , an inhibitor of the ribosomal protein kinase p70S6K ; nor by AG 30 , a selective epidermal growth factor receptor inhibitor . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , PD 184352 did not alter PRL activation of c Myc mRNA expression or stimulation of p70S6K , Akt , and the Jak2 / Stat5 pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In isolated perfused Sprague Dawley rat hearts subjected to 35 min of lethal ischemia , the phosphorylation states of Akt , ERK 1 / 2 , and p 70 S6 kinase ( p70S6K ) were determined after 15 min of reperfusion , and infarct size was measured after 120 min of reperfusion . ^^^ IPC induced a fourfold increase in Akt , ERK 1 / 2 , and p70S6K phosphorylation at reperfusion and reduced the infarct risk to volume ratio ( 56 . 9 + / 5 . 7 and 20 . 9 + / 3 . 6 % for control and IPC , respectively , P < 0 . 01 ) . ^^^ Inhibiting the IPC induced phosphorylation of Akt , ERK 1 / 2 , and p70S6K at reperfusion with the phosphatidylinositol 3 kinase ( PI3K ) inhibitor LY 294002 or the MEK 1 / 2 inhibitor PD 98059 abrogated IPC induced protection ( 46 . 3 + / 5 . 8 , 49 . 2 + / 4 . 0 , and 20 . 9 + / 3 . 6 % for IPC + LY 294002 , IPC + PD 98059 , and IPC , respectively , P < 0 . 01 ) , demonstrating that the phosphorylation of these kinases at reperfusion is required for IPC induced protection . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The PI3K pathway , which can be blocked by wortmannin , leads to phosphorylation of Akt at residues T 308 or S 473 , which then promotes the phosphorylation of p70S6K at T421 / S424 and T 389 . ^^^ Phosphorylation both of Akt and p70S6K is abrogated by pretreatment with pertussis toxin ( PTX ) and an inhibitor of atypical PKCs . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We have now examined the participation of the PI 3 kinase / PDK / Akt / p70s6k signaling cascade in alpha2M * induced cellular proliferation and also studied the role of CREB in these events . ^^^ Silencing of the CREB gene with dsRNA homologous in sequence to the target gene , markedly reduced the levels of CREB mRNA activation of CREB , PI 3 kinase , Akt , and p70s6k in alpha2M * stimulated macrophages . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PURPOSE : To investigate the ability of insulin like growth factor ( IGF ) 1 to prevent apoptosis in lens epithelial cells and the involvement of phosphatidylinositol 3 kinase ( PI 3K ) / Akt and PI 3K / p70 S 6 kinase ( p 70 S6K ) signaling in the cell survival process . ^^^ Stimulation of lens epithelial cells with IGF 1 for 10 minutes to 24 hours resulted in the sustained activation of both Akt and p 70 S6K . ^^^ Furthermore , activation of Akt but not p 70 S6K signaling by IGF 1 resulted in the inhibition of caspase 3 endogenous substrate poly ( ADP ribose ) polymerase ( PARP ) degradation and apoptosis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Using pharmacological inhibitors , we established that PI3K Akt , mTOR p 70 ribosomal protein S 6 kinase ( p70S6K ) , and EKR1 / 2 signaling pathways play a critical role in hypoxia induced adventitial fibroblast proliferation . ^^^ The activation of p70S6K / S6 pathway was sensitive to inhibition by rapamycin and LY 294002 , indicating that mTOR and PI3K / Akt are upstream signaling regulators . ^^^ Thus our data demonstrate that hypoxia induced adventitial fibroblast proliferation requires activation and interaction of PI3K , Akt , mTOR , p70S6K , and ERK1 / 2 and provide evidence for hypoxic regulation of protein translational pathways in cells exhibiting the capability to proliferate under hypoxic conditions . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Moreover , reduced insulinaemia was associated with 4E BP 1 dephosphorylation , enhanced assembly of the 4E BP 1 eIF4E inactive complex and hypophosphorylation of eIF4E , p70S6k and protein kinase B , key intermediates in the regulation of translation initiation and protein synthesis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Investigation of proteins in the phosphatidylinositol 3 ' kinase / Akt signaling pathway in PTEN delivered mouse lung revealed that the PTEN protein was highly expressed , whereas the protein levels of PDK 1 , total Akt 1 , phospho ( Thr 308 ) Akt , phospho ( Ser 2448 ) mTOR , p70S6K , and 4E BP 1 were decreased to varying degrees . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
By using both pharmacologic and genetic approaches , we found that in addition to ERK1 / 2 , phosphatidylinositol 3 kinase ( PI3K ) , Akt , mammalian target of rapamycin ( mTOR ) , and p 70 S6K dependent signaling pathways are required for ATP induced proliferation of adventitial fibroblasts . ^^^ This activation of the mTOR / p70 S 6 kinase ( p 70 S6K ) pathway in response to ATP is because of independent contributions of PI3K / Akt and ERK1 / 2 pathways , which converge on the level of p 70 S6K . ^^^ Collectively , our data demonstrate that ATP induced adventitial fibroblast proliferation requires activation and interaction of multiple signaling pathways such as PI3K , Akt , mTOR , p 70 S6K , and ERK1 / 2 and provide evidence for purinergic regulation of the protein translational pathways related to cell proliferation . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The protein expression of AKT 1 , p70S6K and SHC was higher in islets from pregnant compared with control rats . ^^^ Increased levels of threonine / tyrosine phosphorylation of ERK1 / 2 and serine phosphorylation of AKT and p70S6K were also detected . ^^^ Phosphorylation of AKT was reduced in islets from pregnant and control rats , whereas p70S6K protein levels were reduced only in islets from treated pregnant rats . ^^^ In conclusion , downstream proteins of the PI3K ( AKT and p70S6K ) and MAPK ( SHC and ERK1 / 2 ) cascades are regulated by PRL signaling in islets from pregnant rats . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Rapamycin blocked phosphorylation of p70S6K but had no affect on PDGF induced Akt phosphorylation , positioning p70S6K downstream of Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Catalase induced expression of inflammatory mediators via activation of NF kappaB , PI3K / AKT , p70S6K , and JNKs in BV 2 microglia . ^^^ Interestingly , there was PI3K dependent activation of AKT , p70S6K , JNKs , and NF kappaB in response to catalase . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of p70S6K was also assayed after S 1 P treatment in the presence and absence of inhibitors of PI 3 kinase ( wortmannin , WN , and LY 294002 , LY ) , Akt ( AktI ) , p 38 ( MAPK ) ( SB 203580 ) , and MEK 1 ( PD 98059 ) . ^^^ S 1 P stimulates phosphorylation of p70S6K in a MEK 1 dependent , PI 3 kinase dependent , but Akt independent manner . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
H ( 2 ) O ( 2 ) induced phosphorylation of Akt and p70S6K was dependent on phosphatidylinositol 3 kinase ( PI3K ) activity and was abolished by 1 butanol but not t butanol . ^^^ This study is the first demonstration that PLD 2 activation is implicated in Src dependent phosphorylation of Pyk 2 ( Tyr ( 580 ) and Tyr ( 881 ) ) by promoting the complex formation between Pyk 2 and activated Src in PC 12 cells exposed to H ( 2 ) O ( 2 ) , thereby resulting in activation of the survival signaling pathway PI3K / Akt / p70S6K . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We have previously reported an aberrant accumulation of activated protein kinase B ( PKB ) , glycogen synthase kinase ( GSK ) 3beta , extracellular signal regulated kinase ( ERK1 / 2 ) , c Jun N terminal kinase ( JNK ) , p 38 and p 70 S6 kinase ( p70S6K ) in neurons bearing neurofibrillary tangles ( NFTs ) in Alzheimer ' s disease ( AD ) . ^^^ We found that zinc could induce an increase of phosphorylated ( p ) p70S6K , p PKB , p GSK 3beta , p ERK1 / 2 , p JNK and p p 38 , especially in long term treatment ( 4 8 h ) . ^^^ Thus , 100 microM zinc might activate PKB , GSK 3beta , ERK1 / 2 , JNK , p 38 and p70S6K , that are consequently involved in tau changes in SH SY5Y cells . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Western blot assays revealed that phytosphingosine decreases phosphorylated Akt and p70S6k . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Muscle levels of phosphorylated PKB / Akt and phosphorylated p70S6K returned to Con levels by day 10 of recovery . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This is associated with the depression of activation of the erbB 2 receptor as well as Akt , p70S6K , and ERK 1 / 2 pathways . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Several kinases related to these pathways including protein kinase B ( PKB ) , p 70 S6 kinase ( p70S6K ) , and extracellular signal regulated kinase 1 / 2 ( ERK1 / 2 ) are known cell survival factors and are overactivated in neurons bearing neurofibrillary tangles ( NFTs ) in AD . ^^^ Zinc was used to treat SH SY5Y neuroblastoma cells and effects investigated in relation to PKB , p70S6K , and ERK1 / 2 in the absence and presence of the pro apoptotic agent staurosporine ( STS ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Treatment with Akt inhibitors , but not with those of MEK or p70S6K , blocked the release of the cells from the nocodazole induced G2 / M arrest , further revealing that the Akt activity is required for G2 / M phase transition . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In Ewing sarcoma TC 135 cells , the PDGF BB induced phosphorylation of growth signaling involving extracellular signal regulated kinase , Akt , p70S6K , and the expression of cyclin D 3 were markedly inhibited by transfection with short interfering RNA phospholipase ( PL ) D 2 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin like growth factor 1 mediated skeletal muscle hypertrophy is characterized by increased mTOR p70S6K signaling without increased Akt phosphorylation . ^^^ RESULTS : In the hypertrophic muscle of MLC / mlgf 1 mice , we observed increased phosphorylation of phosphoinositide dependent protein kinase 1 ( PDK 1 ; 53 % increase ) , the mammalian target of rapamycin ( mTOR ; 112 % increase ) , and p 70 S6 kinase ( p70S6K ) ( 254 % increase ) but no significant change in Akt phosphorylation ( 4 % decrease ) . ^^^ CONCLUSION : Persistent overexpression of IGF 1 in mice skeletal muscle results in hypertrophy , which is likely mediated via the mTOR / p70S6K pathway , potentially via an Akt independent signaling pathway . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In this study , we examined the effects of colon cancer associated PIK3CA mutations on the lipid kinase activity in vitro , activation of the downstream targets Akt and p70S6K in vivo and NIH 3T3 transforming ability . ^^^ All the mutants strongly activated Akt and p70S6K compared with wild type p110alpha as determined by immunoblotting using phospho specific antibodies . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In addition , the down regulation of p70S6K could be mediated , at least in part , through activation of AMP activated protein kinase in an Akt independent fashion . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Defects in siRNA IR expressing alpha cells were associated with an alteration in the activity of Akt and p70S6K where insulin induced phosphorylation of protein kinase B / AKt was greatly reduced while p70S6K activation was enhanced , suggesting that the related pathways play important roles in alpha cell function . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , the UV induced signal activation , including phosphorylation of JNK , p 38 kinase , Akt , and p70S6K , was significantly enhanced in p 53 deficient cells ( p 53 / ) , which can be reversed by p 53 reconstitution . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Hepatectomy induced immediate but transient phosphorylation of Akt , p70S6K , mTOR and GSK 3beta in LS 3 KO mice much more than in control mice . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We investigated the pressure induced activation of ribosomal S 6 kinase ( p70S6k ) and its pathway related proteins ( Akt , GSK 3beta , SHP 2 , PTEN ) in aortae from young adult ( 6 month ) , aged ( 30 month ) , and very aged ( 36 month ) Fischer 344 10 Brown Norway F 1 hybrid rats . ^^^ By comparison , the basal phosphorylation of p70S6k at Thr 389 and Thr 421 / Ser 424 was increased ( approximately 40 % ) and unchanged , respectively , while Akt decreased ( approximately 37 % ) , GSK 3beta was unchanged , SHP 2 increased ( approximately 73 . 5 % ) , and PTEN increased ( approximately 120 % ) in the aortae of very aged rats . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We have investigated , in isolated rat adipocytes , the changes caused by GLP 1 , Ex 4 and Ex 9 compared with those provoked by insulin or glucagon , upon the activity of phosphatidylinositol 3 kinase ( PI3K ) , protein kinase B ( PKB ) , p42 / 44 MAP kinases ( MAPKs ) and p70s6 kinase ( p70s6k ) , and the participation of these kinases and protein kinase C ( PKC ) in their action upon 2 deoxy d glucose uptake , lipolysis and lipogenesis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Lovastatin decreases protein kinase B ( PKB ) / Akt phosphorylation , and its downstream effectors , p70S6K and the eukaryotic initiation factor 4E ( eIF4E ) regulatory protein 1 , 4E BP 1 , in a concentration dependent manner , and reduces p70S6K expression . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
However , the HG induced alterations in phosphorylation of Akt , mTOR , p70s6k and GSK 3beta were significantly reversed by IGF 1 . ^^^ Protein expression of Akt , mTOR , p70s6k , GSK 3beta , SERCA2a and phospholamban was unaffected by HG , IGF 1 or rapamycin . ^^^ Collectively , our data suggest that IGF 1 may provide cardiac protection against glucose in part through a PI 3 kinase / Akt / mTOR / p70s6k dependent and calcineurin independent pathway . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We found that KGF induced rapid activation of Akt , p 70 S6K , JNK , and extracellular signal regulated ( ERK ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Cells lacking PDK 1 show decreased activity of these protein kinases , including protein kinase B ( PKB ) and p70S6K , whereas mTOR activity remains largely unaffected . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Here we further characterize this signaling defect and report that a p110delta selective small molecule inhibitor mirrors the effect of genetic inactivation of p110delta in BCR signaling . p110delta activity is indispensable for BCR induced DNA synthesis and phosphorylation of Akt / protein kinase B ( PKB ) , forkhead transcription factor / forkhead box O3a ( FOXO3a ) , and p 70 S6 kinase ( p 70 S6K ) , with modest effects on the phosphorylation of glycogen synthase kinase 3 alpha / beta ( GSK3alpha / beta ) and extracellular signal regulated kinase ( Erk ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Eccentric contractions ( EC ) are known to result in muscle hypertrophy , potentially through activation of the Akt mammalian target of rapamycin p 70 S6 kinase ( p70S6K ) signaling pathway . ^^^ Specifically , we measured the activation of the Akt , GSK 3beta , p70S6K , and ribosomal protein S 6 following a single bout of EC in the rat tibialis anterior ( TA ) muscle . ^^^ EC increased the degree of Akt and p70S6K phosphorylation in the TA muscle , whereas in animals in which SAC had been inhibited , there was a reduced capacity for EC to induce Akt or p70S6K phosphorylation . ^^^ Accompanying this reduced activation of Akt and p70S6K was a failure to phosphorylate GSK 3beta or S 6 when SAC were inhibited . ^^^ The results from these data indicate the necessity of functional SAC for the complete activation of Akt and p70S6K pathway in response to EC . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The cooperative effects of thrombin on Akt / p70S6K phosphorylation and [ ( 3 ) H ] thymidine incorporation were all attenuated by heterologous expression of Gbetagamma sequestrants . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In the cells , insulin induced the phosphorylation of extracellular signal regulated kinases ( Erks ) , Akt at Ser 473 and ribosomal p 70 S6 protein kinase ( p 70 S6K ) at Thr 389 , and the insulin induced 2 deoxy D [ 1 3H ] glucose uptake was inhibited by pre treatment with wortmannin , an inhibitor of phosphatidylinositol 3 kinase ( PI3K ) , or ML 9 , an Akt inhibitor . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The phosphorylation of FAK , mTOR , p70S6K , and PDK 1 were elevated in both breast cancer cell lines , whereas the phosphorylation of AKT , EGFR , ErbB2 / Her2 , PDGFR , Shc , and Stat 3 were elevated in only one breast cancer line compared to normal primary mammary epithelial cells and telomerase immortalised breast epithelial cells . ^^^ Consistent findings were obtained as greater than 70 % of invasive breast carcinomas expressed moderate to high levels of phosphorylated PDK 1 , AKT , p70S6K , and EGFR . ^^^ Elevated phosphorylation of PDK 1 , AKT , mTOR , p70S6K , S 6 , EGFR , and Stat 3 were highly associated with invasive breast tumours ( P < 0 . 05 ) . ^^^ This is the first report demonstrating phosphorylation of PDK 1 is frequently elevated in breast cancer with concomitantly increased phosphorylation of downstream kinases , including AKT , mTOR , p70S6K , S 6 , and Stat 3 . ^^^ This finding thus suggested PDK 1 may promote oncogenesis in part through the activation of AKT and p70S6K and rationalised that PDK 1 as well as downstream components of PDK 1 signalling pathway may be promising therapeutic targets to treat breast cancer . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Treatment of cells with the phosphatidylinositol 3 kinase ( PI3K ) inhibitors wortmannin and LY 294002 [ 2 ( 4 morpholinyl ) 8 phenyl 4H 1 benzopyran 4 one ] or rapamycin , an inhibitor of mammalian target of rapamycin and ribosomal p 70 S6 kinase ( p70S6K ) phosphorylation , or with an adenovirus containing green fluorescent protein and a dominant negative and kinase dead Akt , effectively inhibited the insulin mediated increase in alpha class GST expression and GST activity toward NBD . ^^^ These results show that PI3K / Akt / p70S6K signaling is active in the insulin mediated up regulation of the antioxidant defense system and that low insulin levels , as encountered in diabetes , potentially increase the susceptibility of hepatocytes to xenobiotic mediated and / or oxidative stress mediated damage . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Consistent with observed growth inhibition , PHA 665752 caused cell cycle arrest at G ( 1 ) S boundary accompanied by a dose dependent decrease in phosphorylation of Met , p70S6K , Akt , and extracellular signal regulated kinase 1 / 2 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Reflecting its critical role in integrating cell growth and division with the cellular nutritional environment , the mammalian target of rapamycin * ( mTOR ) is a highly conserved downstream effector of the phosphatidylinositol 3 kinase ( PI3K ) / Akt ( protein kinase B ) signaling pathway . mTOR activates both the 40S ribosomal protein S 6 kinase ( p70s6k ) and the eukaryotic initiation factor 4E binding protein 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
To investigate this hypothesis , skeletal muscles ( ex vivo ) were stimulated with nutrients or intermittent mechanical stretch and the phosphorylation of p70S6k [ P p 70 ( 389 ) ] , PKB [ P PKB ] , mTOR [ P mTOR ( 2481 ) ] , and p 38 [ P p 38 ] was assessed . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , overexpression of p 70 ribosomal S 6 kinase ( p70S6K ) and protein kinase B ( Akt ) enhanced phosphorylation of 4EBP1 and eIF4E binding affinity to the cap region of mRNA . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The Akt / mammalian target of rapamycin ( mTOR ) / ribosomal protein S 6 kinase ( p70S6K ) pathway is considered a central regulator of protein synthesis and of cell proliferation , differentiation , and survival . ^^^ However , the role of the Akt / mTOR / p70S6K pathway in lung carcinoma remains unknown . ^^^ Herein , we explore the role of the Akt / mTOR / p70S6K pathway in fibronectin induced NSCLC cell growth . ^^^ Akt small interfering RNA ( siRNA ) and an antibody against the fibronectin binding integrin alpha5beta1 also blocked the p70S6K phosphorylation in response to fibronectin . ^^^ Taken together , these observations suggest that fibronectin induced stimulation of NSCLC cell proliferation requires activation of the Akt / mTOR / p70S6K pathway and is associated with inhibition of LKB1 / AMPK signaling . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The failure to recover muscle mass in the Ovx group was associated with reduced phosphorylation levels of both Akt and p70s6k , whereas in the Sham recovery animals no reductions were found in Akt phosphorylation and significant increases in p70s6k activation were detected . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PDGF / IL 1beta costimulation also induced a sustained phosphorylation of Akt and p 70 ribosomal S 6 kinase ( p70S6K ) . ^^^ The effects of PDGF / IL 1beta costimulation on contractile marker expression and Akt and p70S6K phosphorylation were blocked by the phosphatidylinositol 3 kinase inhibitors wortmannin and LY 294002 and by adenovirus expressing a dominant negative Akt , and they were mimicked by constitutively active Akt . ^^^ PDGF BB / IL 1beta inhibited the polymerized collagen induced serum response factor DNA binding activity in the nucleus , and this effect was mediated by the PDGFR beta / IL 1R1 association and phosphatidylinositol 3 kinase / Akt / p70S6K pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This was mediated through signaling events involving extracellular signal regulated kinase , phosphatidylinositol 3 kinase / Akt , mammalian target of rapamycin ( mTOR ) , and p70S6K . ^^^ The V659E xenografts also had significantly increased phosphorylated Akt , phosphorylated p70S6K , and VEGF compared with controls . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Taken together , these findings show that rosiglitazone , via up regulation of the PTEN / AMPK and down regulation of the Akt / mTOR / p70S6K signal cascades , inhibits NSCLC cell proliferation through PPARgamma dependent and PPARgamma independent signals . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The PI 3 kinase / Akt pathway and ERK , but not the mTOR / p70s6K pathway account for the suppression of GSK 3beta by bradykinin . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In the hypertrophied noninfarcted left ventricle ( NILV ) , ERK1 / 2 , p 70 S6K , PKB Ser 473 , and Thr 308 phosphorylation were increased . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
KP 1 and KP 2 blocked both the basal and epidermal growth factor induced phosphorylation of Akt Ser 473 at 125 and 250 nmol / L , which , in turn , reduced the activation of intracellular downstream targets of Akt , including GSK 3beta and p70s6k . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The aim of the present study was therefore to examine the effect of TNF alpha pretreatment on glucose uptake and protein synthesis as well as the cellular content and phosphorylation of protein kinase B ( PKB ) , p70S6k , Mitogen Activated Protein ( MAP ) kinase and p90rsk in mouse C2C12 myotubes stimulated with insulin . ^^^ Preincubation of myogenic cells with IL 1beta did not modify either the protein content of PKB and p70S6k or the insulin stimulated phosphorylation of these kinases . ^^^ In conclusion : 1 ) high concentrations of TNF alpha , but not IL beta , present in the extracellular environment during myoblast differentiation prevent the stimulatory action of insulin on glucose uptake and protein synthesis ; 2 ) insulin resistance induced by TNF alpha in C2C12 myogenic cells could be associated with the decreased insulin mediated phosphorylation of PKB and p70s6k , but not with the basal phosphorylation of p42MAPK . . ^^^ Exposure to TNF alpha but not IL 1beta impairs insulin dependent phosphorylation of protein kinase B and p70S6k in mouse C2C12 myogenic cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
INSR substrate 1 , p70S6k , protein kinase B , phosphoinositide dependent protein kinase , Fyn , and glycogen synthase kinase 3 ) after DEX treatment . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Pretreatment of NHEK with PFE ( 60 100 microg / mL ) for 24 h before exposure to UVA resulted in a dose dependent inhibition of UVA mediated phosphorylation of STAT 3 at Tyr 705 , AKT at Ser 473 and ERK1 / 2 . mTOR , structurally related to PI3K , is involved in the regulation of p70S6K , which in turn phosphorylates the S 6 protein of the 40S ribosomal subunit . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The presence of p Akt was accompanied by the phosphorylation of p 27 ( kip 1 ) , FRKHL 1 , MDM 2 , Bad , mTOR , and p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Thyroid hormone stimulates protein synthesis in the cardiomyocyte by activating the Akt mTOR and p70S6K pathways . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Thrombin , histamine , and U 46619 all enhanced EGF stimulated [ 3H ] thymidine incorporation as well as late phase Akt and p70S6K phosphorylation in ASM cultures . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Exposure to a bout of lengthening contractions results in protection from subsequent lengthening contraction induced injury as well as an elevation in phosphorylated Akt and p70S6K . ^^^ Whether Akt or p70S6K is involved in the protection from contraction induced injury is unclear . ^^^ To test for a specific role of Akt and / or p70S6K to induce protective adaptations , we used a conditioning protocol of passive stretches that reduces contraction induced injury with minimal involvement of other cellular responses that have been associated with the Akt signaling pathway , such as increased metabolism , cell growth , and cell death . ^^^ PURPOSE : To determine whether activation of Akt or p70S6K is necessary to induce protective adaptations . ^^^ Phosphorylation of Akt and p70S6K were analyzed by Western blot 0 or 3 h following either lengthening contractions or passive stretches . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We also found that IGF 1 initiated activation of Akt is significantly enhanced after siRNA mediated Gbeta 1 knockdown , while IGF 1 induced p70S6K activation is markedly suppressed following transfection of Gbeta 1 siRNA . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This study showed that PRL stimulated the phosphorylation of mTOR , p70S6K , Akt , and Jak 2 kinases in a dose and time dependent manner in PRL dependent rat Nb 2 lymphoma cells . ^^^ PRL stimulated phosphorylation of mTOR was detected as early as 10 min , closely following the phosphorylation of Akt ( upstream of mTOR ) , but preceding that of the downstream p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
While expression of CA Akt caused a constitutive activation of p70S6 kinase ( p70S6K ) in HC 11 cells , the inhibition of either PI 3 kinase or mTOR abolished the activation of p70S6K by EGF . ^^^ CONCLUSION : PI 3 kinase signaling contributes to the EGF block of lactogenic differentiation via Akt and p70S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Overexpression of Rheb activates 40S ribosomal protein S 6 kinase 1 ( S6K1 ) but not p 90 ribosomal S 6 kinase 1 ( RSK 1 ) or Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Protein kinase B , ribosomal protein S 6 kinase 1 ( S6K1 ) , and eukaryotic initiation factor ( eIF ) 4E binding protein 1 ( 4E BP 1 ) were more phosphorylated , and assembly of the inactive eukaryotic initiation factor 4E . 4E BP 1 complex in muscle and liver was reduced in the fed state ( P < 0 . 001 ) and were not consistently affected by dietary protein level . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This constitutively active form of Akt can also activate p 70 ( S6K ) , indicating that the pleckstrin homology domain is not necessary for downstream interactions . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
IGF 1 activation of phosphoinositide 3 kinase ( PI 3 K ) triggered the activation of two protein kinases , the serine threonine kinase Akt and the p 70 ribosomal protein S 6 kinase ( p 70 ( S6K ) ) . ^^^ Experiments with pharmacological inhibitors , as well as expression of wild type and dominant inhibitory forms of Akt , demonstrated that Akt but not p 70 ( S6K ) mediates PI 3 K dependent survival . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The recombinant BH 1 isoform was phosphorylated by p 70 ribosomal S 6 kinase ( p 70 ( s6k ) ) , mitogen activated protein kinase activated protein kinase 1 , and protein kinase B ( PKB ) , whereas the recombinant BH 3 isoform was a poor substrate for these protein kinases . ^^^ All the protein kinases phosphorylated Ser 466 and Ser 483 in the BH 1 isoform , but to different extents : p 70 ( s6k ) preferentially phosphorylated Ser 466 , whereas mitogen activated protein kinase activated protein kinase 1 and PKB phosphorylated Ser 466 and Ser 483 to a similar extent . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Consistently , Gas 6 activates the P13K downstream targets S6K and Akt , whose activation is abrogated by addition of wortmannin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These data suggest that activation of p 70 ( S6K ) may proceed through a PI 3 kinase and protein kinase B independent but PKC dependent pathway in crystal activated neutrophils . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Use of these cell lines suggests that Rac is involved in both platelet derived growth factor stimulated membrane ruffling and the activation of p 70 ( S6K ) but not in the activation of PKB . ^^^ Furthermore , expression of constitutively active alleles of PKB in PAE cells suggests that PKB is able to regulate the activity of p 70 ( S6K ) but not the cytoskeletal changes underlying membrane ruffling . ^^^ Thus , our results indicate that Rac and PKB are on separate pathways downstream of phosphatidylinositide 3OH kinase in these cells but that both of these pathways are involved in the regulation of p 70 ( S6K ) . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The protein kinases Erk 2 , protein kinase B ( PKB ) , and p 70 ribosomal S 6 kinase ( S6K ) showed no differences in activities in spinal cord tissue between ALS patients and controls . ^^^ However , the amounts of PKB and S6K protein were significantly higher in ALS patients , whereas Erk 2 protein amount was unchanged compared with controls . ^^^ The lack of up regulation in the activities of PKB and S6K in ALS tissue supports an impairment in signal transduction cascades mediated by PI 3 K in this neurodegenerative disease . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Both PGF2alpha and 8 , 12 iso iPF2alpha 3 activate the p70S6 kinase ( p 70 ( S6K ) ) , but not Akt , downstream of phosphatidylinositol 3 kinase ( PI3K ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Following tail vein injection of overnight fasted adult rats with 2 U of insulin per kg body weight , protein kinase B ( PKB ) , the 70 kDa ribosomal S 6 kinase ( S6K ) , and casein kinase 2 ( CK 2 ) were activated ( 30 600 % ) , whereas the MAP / extracellular regulated kinases ( ERK ) 1 and ERK 2 were not stimulated under these conditions . ^^^ When the expression levels of the insulin activated kinases were probed with specific antibodies in ventricular extracts from 1 , 10 , 20 , 50 , and 365 day old rats , phosphatidylinositol 3 kinase ( PI3K ) , PKB , S6K , and CK 2 were downregulated ( 40 60 % ) with age . ^^^ Compared to other adult rat tissues such as brain and liver , the levels of PI3K , PKB , S6K , and GSK3beta were relatively low in the heart . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Protein kinase B , a novel signaling protein kinase , was identified in BTSM cells and was activated by PDGF BB and thrombin in a PtdIns 3 kinase dependent manner ; this may underlie mitogen stimulated activation of p 70 ( s6k ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphoinositide dependent protein kinase 1 ( PDK 1 ) is a recently identified serine / threonine kinase that phosphorylates and activates Akt and p 70 ( S6K ) , two downstream kinases of phosphatidylinositol 3 kinase . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Culture of hepatocytes with TGF beta for 16 hours decreased the stimulation by EGF of ERK 2 and p 70 ( S6k ) ( by 50 % and 35 % , respectively ) , but did not affect the stimulation of either p 38 MAPK , c jun NH 2 terminal kinase ( JNK ) , or protein kinase B ( PKB ) . ^^^ These results suggest that the inhibition of hepatocyte proliferation by TGF beta may be in part mediated by inhibition of ERK 2 and p 70 ( S6k ) , but does not involve PKB , JNK , or p 38 MAPK . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Differential regulation of MAP kinase , p 70 ( S6K ) , and Akt by contraction and insulin in rat skeletal muscle . ^^^ To study the effects of contractile activity on mitogen activated protein kinase ( MAP kinase ) , p 70 S6 kinase ( p 70 ( S6K ) ) , and Akt kinase signaling in rat skeletal muscle , hindlimb muscles were contracted by electrical stimulation of the sciatic nerve for periods of 15 s to 60 min . ^^^ However , insulin , but not contraction , increased p 70 ( S6K ) and Akt activities in the muscle . ^^^ These results demonstrate that contraction induced activation of the MAP kinase pathway is independent of proximal steps in insulin and / or growth factor mediated signaling , and that contraction and insulin have discordant effects with respect to the activation of the MAP kinase pathway vs . p 70 ( S6K ) and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , the phosphorylation of Akt , an upstream effector of both p 70 ( S6k ) and 4E BP phosphorylation , was not affected by eIF4E induction . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In summary , 1 ) the PI3K > PKB > S6K pathway was upregulated under basal conditions , and 2 ) insulin stimulation of PI3K and S6K activities was enhanced , but both PKB and GSK 3 were refractory to the effects of insulin in FF rats . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
During insulin stimulation , IRS 1 and IRS 2 strongly bound p85alpha / beta , which activated phosphatidylinositol ( PI ) 3 kinase , protein kinase B ( PKB ) / Akt , and p 70 ( s6k ) , and promoted the phosphorylation of BAD . ^^^ IRS 4 also promoted the activation of PKB / Akt and BAD phosphorylation during insulin stimulation ; however , it weakly bound or activated p 85 associated PI 3 kinase and failed to mediate the activation of p 70 ( s6k ) . ^^^ Thus , the activation of PKB / Akt and BAD phosphorylation might not be sufficient to inhibit the apoptosis of IL 3 deprived 32D ( IR ) cells unless p 85 associated PI 3 kinase or p 70 ( s6k ) are strongly activated . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Activation of p 70 S6 kinase ( p 70 ( S6K ) ) by growth factors requires multiple signal inputs involving phosphoinositide 3 kinase ( PI3K ) , its effector Akt , and an unidentified kinase that phosphorylates Ser / Thr residues ( Ser ( 411 ) , Ser ( 418 ) , Ser ( 424 ) , and Thr ( 421 ) ) clustered at its autoinhibitory domain . ^^^ Both p 70 ( S6K ) Ser ( 411 ) and Akt Ser ( 473 ) phosphorylation by Ang 2 appear to involve EGF receptor transactivation and were inhibited by dominant negative Ras , whereas the phosphorylation of p 70 ( S6K ) and ERK but not Akt was sensitive to the MEK inhibitor . ^^^ By contrast , the phosphorylation of p 70 ( S6K ) and Akt but not ERK was sensitive to PI3K inhibitors . ^^^ Taken together with the inhibition of Ang 2 induced p 70 ( S6K ) activation by dominant negative Ras and the MEK inhibitor , we conclude that Ang 2 initiated activation of p 70 ( S6K ) requires both ERK cascade and PI3K / Akt cascade that bifurcate at the point of EGF receptor dependent Ras activation . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Immunoblot analyses with phosphospecific antibodies indicated that in addition to MAPK , U 0126 suppressed activation of p 70 ( S6K ) , but not Akt , at concentrations at which it normalized the transformed phenotypes . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These clones were morphologically transformed but Akt and pp 70 ( s6k ) were not constitutively activated in contrast to transient assays and from tumor cell lines deficient in PTEN . ^^^ In addition , the ability of PDGF to induce activation of Akt and pp 70 ( s6k ) was diminished . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
However , no differential activation of STAT 6 , Akt , IRS 2 , or p 70 ( S6k ) , in response to IL 4 , was observed in these cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Hepatocyte swelling also induced wortmannin sensitive activation of PI3K , protein kinase B , and p 70 ( S6K ) . ^^^ Taken together , these results indicate that 1 ) cell swelling stimulates TC uptake by translocating Ntcp to the plasma membrane , 2 ) this effect is mediated via the PI3K , but not MAPK , signaling pathway , and 3 ) protein kinase B , but not p 70 ( S6K ) , is a likely downstream effector of PI3K . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Thus , in contracting skeletal muscle , insulin stimulates glucose uptake and activates PKB , but not p 70 ( S6K ) , by a PI 3 kinase dependent mechanism that is independent of changes in IRS 1 and IRS 2 associated PI 3 kinase activity . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We show that phosphatidylinositol 3 kinase ( PI3K ) / Akt and p 70 ( S6K ) are crucial signaling molecules mediating the stimulatory effect of IGFs on myogenin expression . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Amino acids stimulate p 70 ( s6k ) and transiently inhibit glycogen synthase kinase 3 without effects on the activity of protein kinase B or the mitogen activated protein kinase pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin stimulation of two kinases downstream from PI 3 kinase , Akt and p 70 S6 kinase ( p 70 ( S6K ) ) , was decreased in cells expressing p85alpha or AS 53 but not in cells expressing p50alpha . ^^^ Similar inhibition of PI 3 kinase , Akt , and p 70 ( S6K ) was observed , even when p110alpha was coexpressed with p85alpha or AS 53 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
I+P and PMA equally stimulated phosphorylation of ERK1 / 2 , but I+P more strongly stimulated Akt , and p 70 ( S6K ) phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The effects of PKC on Akt were transmitted through the PI 3K cascade as indicated by changes in p 70 s6 kinase ( p 70 ( s6k ) ) phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Reduction in PDK 1 levels resulted in inhibition of PKB activity , and a reduction in phosphorylation on Thr 308 and Ser 473 of PKB . p 70 S6 kinase ( p 70 ( S6K ) ) activity was also reduced . ^^^ This study confirms both PKB and p 70 ( S6K ) as in vivo substrates for PDK 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
A mutant of Akt that retains kinase activity but does not induce phosphorylation of S6K or of 4E BP 1 fails to transform chicken embryo fibroblasts , suggesting a correlation between the oncogenicity of Akt and phosphorylation of S6K and 4E BP 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Growth factor stimulated phosphorylation of Akt and p 70 ( S6K ) is differentially inhibited by LY 294002 and Wortmannin . ^^^ These compounds inhibit the kinase action of PI3K , thus preventing the accumulation of PI ( 3 , 4 , 5 ) P 3 and PI ( 3 , 4 ) P 2 ( PIs ) and subsequent phosphorylation and activation of the downstream effectors of PI3K , Akt and p 70 ( S6K ) . ^^^ However , their effects on activation of Akt and p 70 ( S6K ) , more widely used markers of PI3K activation , has not been formally tested . ^^^ We have examined the effects of LY and WM on phosphorylation of Akt and p 70 ( S6K ) by insulin like growth factor 1 , insulin , and platelet derived growth factor in skeletal muscle cells . ^^^ LY is much less effective in blocking the phosphorylation of Akt than p 70 ( S6K ) ; at concentrations which completely inhibit phosphorylation of p 70 ( S6K ) , phosphorylation of Akt is only partially inhibited by LY . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Alterations of Akt 1 ( PKBalpha ) and p 70 ( S6K ) in transient focal ischemia . ^^^ One of the potential downstream targets of Akt 1 is p 70 S6 kinase , p 70 ( S6K ) , an enzyme implicated in the regulation of protein synthesis . ^^^ In this study , we investigated the changes in total and phosphorylated levels of Akt 1 and p 70 ( S6K ) during transient focal ischemia . ^^^ The expression of total and phosphorylated forms of Akt 1 and p 70 ( S6K ) were examined by Western blot analysis . ^^^ The results show that cell survival pathways , such as Akt 1 and p 70 ( S6K ) signaling , are suppressed after transient focal ischemia , which may contribute to the development of neuronal cell death after an ischemic insult . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Examination of the signaling components downstream of PI3K , 3 phosphoinositide dependent kinase 1 , protein kinase B ( PKB ) , glycogen synthase kinase 3 , and p 70 kDa S 6 kinase ( p 70 ( S6K ) ) , suggested that a major part of glucose dependent beta cell proliferation requires activation of mammalian target of rapamycin / p70 ( S6K ) , independent of phosphoinositide dependent kinase 1 / PKB activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
A prolonged increase in p 70 ( S6k ) and a transient increase in protein kinase B phosphorylation were only observed in response to a growth inducing stimulus ( e . g . , tibialis anterior in high frequency electrical stimulation ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
FGF 2 stimulates the activation of the PI 3 K , P 70 ( S6K ) and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Recent studies indicate that zinc activates p 70 S6 kinase ( p 70 ( S6k ) ) by a mechanism involving phosphatidylinositol 3 kinase ( PI 3 kinase ) and Akt ( protein kinase B ) . ^^^ However , in contrast to insulin , amino acids activate p 70 ( S6k ) by an unknown PI 3 kinase and Akt independent mechanism . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Gas 6 is the ligand of Axl receptor tyrosine kinase ; upon binding to its receptor Gas 6 activates the phosphatidylinositol 3 OH kinase ( PI3K ) and its downstream targets S6K and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
H 89 blocks MSK 1 activity but does not inhibit ultraviolet B induced activation of MAP kinases p70 / 85 ( S6K ) , p 90 ( RSK ) , Akt , and protein kinase A . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
To test the hypothesis that leucine and insulin stimulate translation initiation in human skeletal muscle by phosphorylating 70 kDa ribosomal protein S 6 kinase ( p 70 ( S6k ) ) , we infused healthy adults with leucine alone ( n = 6 ) , insulin alone ( n = 6 ) , or both leucine and insulin ( n = 6 ) for 2 h . p 70 ( S6k ) and protein kinase B ( PKB ) serine ( 473 ) phosphorylation were measured in vastus lateralis muscles . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The PIF binding pocket in PDK 1 is essential for activation of S6K and SGK , but not PKB . ^^^ PDK 1 activates S6K , SGK and PKB isoforms by phosphorylating these kinases at their T loop . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
S1P ( 100 nM ) increased the phosphorylation of p42 / 44MAPK , p38MAPK , JNK , Akt and p 70 ( S6K ) , this effect being reversed by inhibitors of their respective phosphorylation which also rescue the hypertrophic phenotype . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Wortmannin , LY 294002 , and rapamycin at concentrations that did not affect MAPK phosphorylation but substantially inhibited PI3K , Akt , and p 70 ( S6K ) significantly suppressed the soft agar growth of tumor cell lines that overexpress ErbB 2 but not the growth of tumor lines with low ErbB 2 expression . ^^^ Our results indicate that the PI3K / Akt / p70 ( S6K ) pathway plays an enhanced role in the anchorage independent growth of ErbB 2 overexpressing breast cancer cells , therefore providing a molecular basis for the selective targeting of this signaling pathway in the treatment of ErbB 2 related human breast malignancies . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In the present study , we used effector domain mutants of the constitutively activated Rac ( 61L ) mutant that display differential transforming activities and differential activation of downstream effector pathways to investigate the contribution of p 70 S6 kinase ( p 70 ( S6K ) ) to Rac 1 transformation and to decipher the signaling pathways leading from Rac 1 to p 70 ( S6K ) . ^^^ First , we found that Rac 1 transforming activity could be dissociated from Rac 1 activation of p 70 ( S6K ) . ^^^ A weakly transforming Rac 1 mutant retained the ability to activate p 70 ( S6K ) , whereas some potently transforming effector mutants were impaired in their ability to activate p 70 ( S6K ) . ^^^ These data suggest that p 70 ( S6K ) is not necessary to promote full Rac 1 transforming activity . ^^^ We also found a strong correlation between the ability of the Rac ( 61L ) effector mutants to activate p 70 ( S6K ) and their ability to activate the JNK mitogen activated protein kinase . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PDK 1 regulates growth through Akt and S6K in Drosophila . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt 1 and p 70 ( s6k ) appeared to be important downstream targets of IGFR 1 mediated resistance to anti EGFR targeting . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Regulation of cell size in growth , development and human disease : PI3K , PKB and S6K . ^^^ Here we focus on two components of this pathway , PKB and S6K , and briefly review the experiments that initially uncovered their roles in cell size control . ^^^ Finally , we have utilized two contemporary studies involving PKB and S6K deficient mice as a paradigm to underscore the importance of cell size and to accurately delineate the connections between signaling pathways for human disease , such as diabetes mellitus . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Because activation of the PI 3 K / AKT as well as RAS MEK ERK pathways may result in downstream stimulation of the p 70 ( S6K ) ( p 70 ) and phosphorylation of the 4E BP 1 translational repressor , we assessed these potential molecular targets in IL 6 treated myeloma cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of p 70 ( S6K ) was also increased by IGF 1 / glucose , but not by TGF alpha / EGF , despite upstream PKB activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Nordihydroguaiaretic acid had no inhibitory effect on growth and survival signals such as tyrosine phosphorylation of the epidermal growth factor receptor or basal and growth factor stimulated activities of extracellular signal regulated kinase 1 / 2 , p 70 ( s6k ) and AKT but selectively inhibited expression of cyclin D 1 in the cancer cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of p70 / p85 ( S6K ) coincided with protein kinase B and GSK 3beta phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The AGC family of protein kinases , which includes isoforms of protein kinase B ( also known as Akt ) , ribosomal S 6 protein kinase ( S6K ) , and serum and glucocorticoid induced protein kinase ( SGK ) are activated in response to many extracellular signals and play key roles in regulating diverse cellular processes . ^^^ This study provides the first description of the basis for the substrate specificity of NEK 6 and indicates that NEK 6 is unlikely to be responsible for the IGF 1 induced phosphorylation of the hydrophobic motif of S6K , SGK , and protein kinase B isoforms in vivo . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PDK 1 functions as a master kinase , phosphorylating and activating PKB / Akt , S6K and RSK . ^^^ In contrast , hypomorphic PDK 1 mice are viable and fertile , and insulin injection induces the normal activation of PKB , S6K and RSK . ^^^ We provide genetic evidence that PDK 1 is essential for mouse embryonic development , and regulates cell size independently of cell number or proliferation , as well as insulin ' s ability to activate PKB , S6K and RSK . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Treatment of cells with UV radiation or H2O2 also markedly activated Erks , JNKs , p 38 kinase and led to increases in phosphorylation of Akt and p 70 ( S6k ) in mouse epidermal JB 6 cells . ^^^ The scavenging of UV generated H2O2 by N acety L cyteine ( NAC , a general antioxidant ) or catalase ( a specific H2O2 inhibitor ) inhibited UV induced activation of JNKs , p 38 kinase , Akt and p 70 ( S6k ) , while it did not show any inhibitory effects on Erks activation . ^^^ These results demonstrate that H2O2 generation is required for UV induced phosphorylation of Akt and p 70 ( S6k ) , and involved in activation of JNKs and p 38 kinase , but not Erks . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin increased the phosphorylation of p 70 S6 kinase ( p 70 ( S6k ) ) in both muscle and liver and protein kinase B ( PKB / Akt ) in muscle , two indicative signal proteins in the phosphatidylinositol ( PI ) 3 kinase pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Similar to Akt , phosphorylation of p70S6 kinase ( p 70 ( S6K ) ) by IGF 1 was also enhanced in +BP3 cells relative to Mock cells at both 15 min and 10 h . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Consistent with these results , we show that RV attenuates phosphorylation of the p 70 ribosomal protein S 6 kinase ( p 70 ( S6K ) ) , a kinase downstream of the ERK 1 / 2 as well as the Akt pathway , that is implicated in Ang 2 induced protein synthesis . ^^^ In summary , we demonstrate for the first time that RV inhibits Ang 2 induced VSMC hypertrophy , possibly by interfering mainly with the PI ( 3 ) K / Akt and p 70 ( S6K ) but also with the ERK 1 / 2 signaling pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In both cell lines , constitutive activation of the PI 3 K / Akt / FKHRL 1 , mTOR / P70 ( S6K ) and MAPK pathways was detected . ^^^ LY 294002 inhibited phosphorylation of Akt , FKHRL 1 and P 70 ( S6K ) but had no effect on ERK1 / 2 phosphorylation , indicating that the PI 3 K and MAPK pathways are independent . ^^^ IGF 1 but not IL 6 increased phosphorylation of Akt , FKHRL 1 and P 70 ( S6K ) . ^^^ In three of them including the two patients with PCL , constitutive phosphorylation of Akt , FKHRL 1 and P 70 ( S6K ) was present , inhibited by LY 294002 and enhanced by IGF 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The growth factor activated AGC protein kinases RSK , S6K , PKB , MSK and SGK are activated by serine / threonine phosphorylation in the activation loop and in the hydrophobic motif , C terminal to the kinase domain . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Ultraviolet induced phosphorylation of p 70 ( S6K ) at Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) involves hydrogen peroxide and mammalian target of rapamycin but not Akt and atypical protein kinase C . ^^^ Importantly , UV induced increases in p 70 ( S6k ) phosphorylation at Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) were dramatically inhibited by pretreatment of cells with rapamycin , LY 294002 , or PD 98059 , whereas overexpression of dominant negative mutants of PKClambda / iota and Akt 1 did not inhibit p 70 ( S6k ) phosphorylation at Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) . ^^^ These results demonstrated that H ( 2 ) O ( 2 ) , phosphatidylinositol 3 kinase , and mammalian target of rapamycin were important players for UV induced p 70 ( S6k ) phosphorylation at Thr ( 389 ) and Thr ( 421 ) / Ser ( 424 ) , whereas Akt and atypical protein kinase C were not involved in this activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Rectus muscle protein synthesis was measured at the end of the clamp , and the phosphorylation states of protein kinase B ( Akt ) , eukaryotic initiation factor 4E binding protein 1 ( 4E BP 1 ) , and ribosomal protein S 6 kinase ( p 70 ( S6K ) ) were quantitated before and after the insulin clamp . ^^^ The basal phosphorylation states of Akt , 4E BP 1 , and p 70 ( S6K ) were similar between ADX and Sham rats . ^^^ Insulin significantly enhanced the phosphorylation of Akt ( P < 0 . 03 ) , 4E BP 1 ( P = 0 . 003 ) , and p 70 ( S6K ) ( P < 0 . 002 ) in ADX but not in Sham rats . ^^^ Glucocorticoid replacement blunted the effect of insulin on Akt , 4E BP 1 , and p 70 ( S6K ) phosphorylation and protein synthesis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Transfection of PTEN into the PC 3 cells decreased the activation of Akt and the downstream mTOR regulated 70 kDa S 6 ( p 70 ( s6k ) ) kinase and reversed the resistance to doxorubicin in these cells , indicating that changes in PTEN status / Akt activation modulate the cellular response to doxorubicin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Forearm muscle protein synthesis and degradation ( phenylalanine tracer method ) and the phosphorylation of protein kinase B ( or Akt ) , eukaryotic initiation factor 4E binding protein 1 , and ribosomal protein S 6 kinase ( p 70 ( S6K ) ) in vastus lateralis muscle were measured before and after AA infusion . ^^^ AA did not activate Akt phosphorylation at Ser ( 473 ) , but significantly increased the phosphorylation of both eukaryotic initiation factor 4E binding protein 1 ( P < 0 . 04 ) and p 70 ( S6K ) ( P < 0 . 001 ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Activated Akt increased phosphorylation of downstream substrates such as GSK 3 , p 70 ( S6K ) , 4EBP 1 , and FKHR . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Okadaic acid ( OA ) inhibited the FTY 720 induced dephosphorylation of Akt and p 70 ( S6k ) , suggesting that FTY 720 promotes Ser / Thr protein phosphatase ( PP ) activity . 6 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Here we demonstrate the ability of DeltaMEK 1 : ER to activate the phosphatidylinositol 3 kinase ( PI3K ) / Akt / p70 ribosomal S 6 kinase ( p 70 ( S6K ) ) pathway and the importance of this pathway in MEK 1 mediated prevention of apoptosis . ^^^ Stimulation of DeltaMEK 1 : ER by 4HT resulted in ERK , PI3K , Akt and p 70 ( S6K ) activation . ^^^ Treatment with PI3K , Akt and p 70 ( S6K ) inhibitors prevented MEK responsive growth . ^^^ Furthermore , the apoptotic effects of PI3K / Akt / p70 ( S6K ) inhibitors could be enhanced by cotreatment with MEK inhibitors . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We have shown further that S 6 kinase ( S6K ) is a downstream component of the PI3K / Akt / TSC pathway and reduction of S6K activity can block TSC defects . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PKB / Akt , S6K , SGK and RSK are mediators of responses triggered by insulin and growth factors and are activated following phosphorylation by 3 phosphoinositide dependent protein kinase 1 ( PDK 1 ) . ^^^ These experiments establish the importance of the PIF pocket in governing the activation of S6K , RSK , SGK , but not PKB , in vivo . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
AKT , extracellular signal regulated kinase 1 / 2 ( ERK1 / 2 ) , and p 70 ( s6k ) were simultaneously activated after the HGF stimulation , peaking at 30min after the treatment . ^^^ The activation of AKT , p 70 ( s6k ) , and ERK1 / 2 induced by HGF was abolished by pre treatment with LY 294002 , a phosphoinositide 3 OH kinase ( PI3K ) inhibitor , and U 0126 , a mitogen activated protein kinase / ERK kinase ( MEK ) inhibitor , respectively . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Insulin did not activate PKB and S6K , nor did it stimulate 6 phosphofructo 2 kinase and production of fructose 2 , 6 bisphosphate , in the hearts of mPDK 1 ( / ) mice , consistent with PDK 1 mediating these processes . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The cytokine signaling intermediates for mTOR / ribosomal protein S 6 kinase ( S6K ) activation include phosphatidylinositol 3 kinase , Akt , Erks and geranylgeranylated proteins . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
PI3K regulates cell cycle through AKT , mTOR to p 70 ( S6K ) . ^^^ These results suggest that PI3K mediates G ( 1 ) cell cycle progression and cyclin expression through the activation of AKT / mTOR / p70 ( S6K ) signaling pathway in the prostate cancer cells . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , IGF 1 still induced normal phosphorylation of WNK 1 in PDK 1 ( L155E / L155E ) knock in ES cells in which PKB , but not S6K ( p 70 ribosomal S 6 kinase ) or SGK 1 ( serum and glucocorticoid induced protein kinase 1 ) , is activated . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Replacing Ser ( 302 ) with alanine significantly reduced insulin stimulated tyrosine phosphorylation of IRS 1 and p 85 binding and reduced insulin stimulated phosphorylation of p 70 ( S6K ) , ribosomal S 6 protein , and 4E BP 1 ; however , this mutation had no effect on insulin stimulated Akt or glycogen synthase kinase 3beta phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
ADX had no effect on myocardial Akt or GSK 3 [ glycogen synthase ( GS ) kinase 3 ] phosphorylation , but it decreased the phosphorylation of eukaryotic initiation factor 4E binding protein 1 ( 4E BP 1 ) and ribosomal protein S 6 kinase ( p 70 ( S6K ) ) ( P < 0 . 003 for both ) . ^^^ Insulin enhanced the phosphorylation of Akt ( P < 0 . 04 ) , 4E BP 1 ( P < 0 . 002 ) , and p 70 ( S6K ) ( P < 0 . 0001 ) in ADX , but not in sham rats . ^^^ Dexamethasone restored the levels of 4E BP 1 and p 70 ( S6K ) phosphorylation and abrogated the insulin stimulated Akt , 4E BP 1 , and p 70 ( S6K ) phosphorylation . ^^^ We conclude that endogenous glucocorticoids differentially modulate the regulation of Akt 4E BP1 / p70 ( S6K ) and Akt GSK 3 GS signaling pathways in heart by physiologic hyperinsulinemia over a range from deficiency to physiological stress concentrations . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Signaling from Akt to FRAP / TOR targets both 4E BP and S6K in Drosophila melanogaster . ^^^ Although S6K phosphorylation is independent of phosphoinositide 3 OH kinase ( PI3K ) and serine / threonine protein kinase Akt , that of 4E BP is dependent on PI3K and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Nickel compounds act through phosphatidylinositol 3 kinase / Akt dependent , p 70 ( S6k ) independent pathway to induce hypoxia inducible factor transactivation and Cap 43 expression in mouse epidermal Cl 41 cells . ^^^ The present study indicated that exposure of mouse epidermal Cl 41 cells to either Ni ( 3 ) S ( 2 ) or NiCl ( 2 ) resulted in activation of phosphatidylinositol 3 kinase ( PI 3K ) , Akt , and p 70 S6 kinase ( p 70 ( S6k ) ) . ^^^ Inhibition of PI 3K , Akt , and p 70 ( S6k ) by overexpression of a dominant negative mutant of PI 3K ( Deltap 85 ) impaired nickel induced HIF 1 transactivation . ^^^ Furthermore , an overexpression of the dominant negative Akt mutant ( Akt T308A / S473A ) blocked nickel induced Akt phosphorylation and HIF 1 transactivation , whereas inhibition of p 70 ( S6k ) activation by pretreatment of cells with rapamycin did not show significant inhibitory effects on HIF 1 transactivation induced by nickel compounds . ^^^ These results demonstrated that nickel compounds induce HIF 1 transactivation and Cap 43 protein expression through a PI 3K / Akt dependent and p 70 ( S6k ) independent pathway . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Toxin B , which inactivates Rho GTPases , markedly impaired PLD 1 activation and phosphorylation of Akt , p 70 ( S6K ) , and 4E BP 1 induced by LPA but had a minimal or no effect on the actions of PDGF . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Another novel observation of this study was that there were also decreases in total protein levels of p 38 MAPK , p 70 ( S6K ) , JNK , and Akt following beta AR blockade . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Additionally , most GISTs showed activation of MAPK p42 / 44 , AKT , S6K , STAT 1 , and STAT 3 . ^^^ Using GIST in vitro models , we showed that activation of MAPK p42 / 44 , AKT , and S6K was KIT dependent , whereas STAT 1 and STAT 3 phosphorylation was only partially dependent on KIT activation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Western blot analysis showed that SPE reduced IGF 1 induced phosphorylation of the adapter protein insulin receptor substrate 1 and decreased downstream effects of Akt activation , including increased cyclin D 1 levels and phosphorylation of glycogen synthase kinase 3 and p 70 ( s6k ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , we found that Akt is a PI 3K downstream mediator for 5 MCDE induced AP 1 transactivation , whereas another PI 3K downstream kinase , p 70 ( S6K ) , was not involved in AP 1 activation by 5 MCDE . ^^^ These results demonstrate that 5 MCDE is able to induce AP 1 activation , and the AP 1 induction is specifically through a PI 3K / Akt dependent and p 70 ( S6K ) independent pathway . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Interestingly , amino acids and Rheb , but not IGF 1 , activated S6K in the knockin cells , supporting the idea that PtdIns ( 3 , 4 , 5 ) P 3 stimulates S6K through PKB mediated activation of Rheb . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
By contrast , the major translational control pathway involving Akt , mTOR , and S6K was strongly regulated by fasting and refeeding . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
MATERIALS AND METHODS : Levels of expression of PI3K pathway members were assessed in 92 prospectively collected gliomas through quantitative Western analysis using total and phospho specific antibodies for PI3K , Akt , and p 70 ( s6k ) . ^^^ Levels of phospho PI3K , phospho Akt , and phospho p 70 ( s6k ) were all found to be inversely associated with cleaved caspase 3 levels , suggesting PI3K pathway activation is associated with reduced levels of apoptosis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Immunocytochemical studies showed that p 70 ( S6K ) , Akt 1 , PDK 1 , and p 85 phosphoinositide 3 kinase ( PI 3 kinase ) were localized to the actin arc , a caveolin enriched cytoskeletal structure located at the leading edge of migrating cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Analyses of signaling molecules upstream of CDK4 / 6 revealed that S 6 kinase ( S6K ) activation was affected by PILSAP , whereas that of phosphatidylinositol 3 kinase ( PI3K ) , Akt , and extracellular signal related kinase 1 / 2 ( ERK1 / 2 ) was not . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
One of the most studied signalling events controlled by PtdIns ( 3 , 4 , 5 ) P 3 , comprises the activation of a group of AGC family protein kinases , including isoforms of protein kinase B ( PKB ) / Akt , p 70 ribosomal S 6 kinase ( S6K ) , serum and glucocorticoid induced protein kinase ( SGK ) and protein kinase C ( PKC ) , which play crucial roles in regulating physiological processes relevant to metabolism , growth , proliferation and survival . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Concordant phosphorylation of downstream targets of Akt , glycogen synthase kinase 3beta ( GSK 3beta ) and p 70 ribosomal S 6 kinase ( p 70 ( S6K ) ) , in response to Akt activation was observed at 15 min after pressure overload . ^^^ However in volume overloaded hearts , phosphorylation of GSK 3beta and p 70 ( S6K ) was observed at 6 weeks and at 6 and 12 weeks , respectively , and was not coincident with Akt activation . ^^^ These findings suggest that phosphorylation of GSK 3beta and p 70 ( S6K ) is regulated by an alternative pathway other than Akt in volume overloaded hearts . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Both types of stretch induced an increase in extracellular signal regulated kinase ( ERK ) and protein kinase B ( PKB / Akt ) phosphorylation , but only multiaxial stretch induced ribosomal S 6 kinase ( p 70 ( S6k ) ) phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The rapid activation of PI3K Akt / PKB mTOR p 70 ( S6K ) cascade by T 3 provides a new molecular mechanism for thyroid hormone action . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Akt mammalian target of rapamycin S6k and NF kappaB inducing kinase ( NIK ) NF kappaB axis are the two main signaling pathways regulating cell survival and inflammation . ^^^ However , in rapamycin treated patients , a significant reduction of S6k but not Akt and NIK activation was observed . ^^^ A time dependent activation of phosphatidylinositol 3 kinase , Akt , S6k , and NIK was observed in the experimental model with the same pattern reported for transplant recipients who did not receive rapamycin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Combined treatment also resulted in pronounced reductions in levels of phospho Akt , glycogen synthase kinase 3 ( GSK 3 ) , p 70 ( S6K ) , mammalian target of rapamycin ( mTOR ) , forkhead transcription factor ( FKHR ) , caspase 9 , and Bad . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The antisurvival effects of luteolin were mediated via blockage of PI3K / Akt dependent pathways , whereas inhibition of the PI3K / p70 S6K pathway mediated the antimitotic effects of the compound . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Balancing Akt with S6K : implications for both metabolic diseases and tumorigenesis . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Growth inhibition is associated with a reduction in S6K but not PKB / Akt activity . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This family includes protein kinase C ( PKC ) , protein kinase B ( PKB ) , p70 / p90 ribosomal S 6 kinases ( RSK and S6K ) , and the catalytic subunit of cAMP dependent protein kinase ( PKA ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Several KIT activating mutations , which are largely responsible for the development of this tumor , promote cell survival , proliferation , and migration through different pathways such as MAPK p42 / 44 , AKT , S6K , STAT 1 , and STAT 3 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In addition , radicicol , an inhibitor of heat shock protein 90 ( Hsp 90 ) , and rapamycin , an inhibitor of the mammalian target of rapamycin ( mTOR ) , blocked IL 2 induced hTERT activity and nuclear translocation of hTERT but not hTERT mRNA expression . hTERT was coimmunoprecipitated with Akt , Hsp 90 , mTOR , and p 70 S6 kinase ( S6K ) , suggesting that these molecules form a physical complex . ^^^ Immunoprecipitates of Akt , Hsp 90 , mTOR , and S6K from IL 2 stimulated NK 92 cells contained telomerase activity . ^^^ These results indicate that IL 2 stimulation induces hTERT activation and that the mechanism of IL 2 induced hTERT activation involves transcriptional or posttranslational regulation through the pathway including PI3K / Akt , Hsp 90 , mTOR , and S6K in NK cells . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Basal levels of Akt and its target p 70 ( S6K ) remained constant regardless of treatment . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In conclusion , adrenaline potentiates insulin stimulated activation of PKB and p 70 ( S6K ) via cAMP and Epac in skeletal muscle . ^^^ Furthermore , the fact that adrenaline alone did not activate PKB or p 70 ( S6K ) suggests that a hormone can be a potent regulator of signalling despite no effects being seen when co activators are lacking . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In human lung epithelial adenocarcinoma ( A 549 ) cells , LY 303511 , like rapamycin , inhibited mTOR dependent phosphorylation of S6K , but not PI3K dependent phosphorylation of Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
These effects of IGF 1 were associated with increased phosphorylation of Akt , GSK 3beta , and the mTOR downstream targets p 70 ( S6K ) and 4E BP 1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
RESULTS : Simultaneous exposure of myeloma cells to marginally toxic concentrations of L 744832 and UCN 01 resulted in a synergistic induction of mitochondrial damage , caspase activation , and apoptosis , associated with activation of p34cdc2 and c Jun NH 2 kinase and inactivation of extracellular signal regulated kinase , Akt , GSK 3 , p 70 ( S6K ) , and signal transducers and activators of transcription 3 ( STAT 3 ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We now know that three of the most frequent mutations in cancer constitutively activate PI3Kalpha and , when expressed in cells , they drive the oncogenic transformation and chronic activation of downstream signalling by molecules such as PKB , S6K and 4E bp 1 that is commonly seen in cancer cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Compared with control cells , HUVEC overexpressing T cad ( T cad+ HUVEC ) had higher phosphorylation levels for phosphatidylinositol 3 kinase ( PI3K ) target Akt and mTOR target p 70 ( S6K ) ( survival pathway regulators ) , but lower levels for p38MAPK ( death pathway regulator ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We have examined the basal and insulin mediated phosphorylation of protein kinase B ( PKB ) , protein kinase Czeta ( PKCzeta ) , p 70 ( S6k ) , mitogen activated protein kinase ( MAPK ) / p90 ( rsk ) pathway and the expression of IGFBP 3 , 4 , and 5 in mice selected for body weight gain ( line C ) and reduction ( line L ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In conclusions : 1 ) high glucose abolishes the stimulatory action of IGF 1 on protein synthesis and it does not affect the activation of PKB , p 70 ( S6k ) , and p 90 ( rsk ) in mouse C2C12 myogenic cells , 2 ) high glucose with high insulin in combination also abolish the stimulatory effect of IGF 1 , but this phenomenon is accompanied by attenuated PKB and p 70 ( S6k ) activation and the lack of activation of p 90 ( rsk ) , 3 ) apart from PKB , p 70 ( S6k ) and p 90 ( rsk ) , other kinases are probably involved in the regulation of IGF 1 mediated protein synthesis in myogenic cells . . ^^^ The impairment of IGF 1 stimulated protein synthesis and activation of protein kinase B , p 70 ( S6k ) , MAP kinase , and p 90 ( rsk ) in mouse C2C12 myogenic cells exposed to high glucose and high insulin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , sustained glutamatergic stimulation inhibits ERK , Akt , and S6K . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Many cancers possess elevated levels of PtdIns ( 3 , 4 , 5 ) P ( 3 ) , the second messenger that induces activation of the protein kinases PKB / Akt and S6K and thereby stimulates cell proliferation , growth , and survival . ^^^ Cells lacking PTEN possess elevated levels of PtdIns ( 3 , 4 , 5 ) P ( 3 ) , PKB , and S6K activity and heterozygous PTEN ( + / ) mice develop a variety of tumors . ^^^ We explored the importance of PDK 1 , the protein kinase that activates PKB and S6K , in mediating tumorigenesis caused by the deletion of PTEN . ^^^ Our findings provide genetic evidence that PDK 1 is a key effector in mediating neoplasia resulting from loss of PTEN and also validate PDK 1 as a promising anticancer target for the prevention of tumors that possess elevated PKB and S6K activity . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We hypothesized a differential activation of the anabolic signaling proteins protein kinase B ( PKB ) and p 70 S6 kinase ( p 70 ( S6K ) ) and subsequent differential stimulation of human muscle protein synthesis ( MPS ) after dynamic shortening or lengthening exercise . ^^^ PKB and p 70 ( S6K ) phosphorylation increased approximately 3 fold after 3 h and remained elevated at 6 and 24 h . ^^^ Short term dynamic exercise in either shortening or lengthening mode increases MPS at least as much as resistance exercise and is associated with long term activation of PKB and p 70 ( S6K ) . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
By dissecting the downstream signals necessary for this event , we found that Rac1 / p38 and Akt are required , whereas the c Jun N terminal kinase ( JNK ) and mTOR / p70 ( s6k ) pathways are dispensable . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We found that exposure of Cl 41 cells to arsenite was able to induce cell proliferation , activate PI 3K > Akt / p70 ( S6k ) signal pathway and increase cyclin D 1 expression at both transcription and protein levels . ^^^ Pre treatment of Cl 41 cells with PI 3K inhibitor , wortmannin , significantly inhibited the phosphorylation of Akt and p 70 ( S6k ) and thereby dramatically impaired the cyclin D 1 induction by arsenite , implicating the importance of the PI 3K signal pathway in the cyclin D 1 induction by arsenite . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Consistent with inhibition of AP 1 activation , the RO ME fraction markedly inhibited activation of PI 3K , Akt , and p 70 S6 kinase ( p 70 ( S6k ) ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Likewise , activation of molecules associated with hypertrophy ( AKT , mTOR , and p 70 ( S6k ) ) was diminished in mice overexpressing integrin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Further biochemical analysis revealed that the activation of the PI3K AKT mammalian target of the rapamycin p 70 ( S6K ) pathway was observed in both the cytoplasmic and nuclear compartments , whereas the activation of the PI3K integrin linked kinase matrix metalloproteinase 2 pathway was detected mainly in the extranuclear compartments . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The invasive / migratory phenotype activated by HGF can be blocked by specific inhibitors of the phosphatidylinositol 3 kinase ( PI3K ) cascade , inhibitor of p 70 ( S6K ) , and also the expression of a dominant negative Akt , demonstrating that HGF transmits the motogenic signal through PI3K and Akt to p 70 ( S6K ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Here we investigated the expression of atrogin 1 , MuRF 1 , and the activity of Akt and its catabolic ( FKHR and FKHRL 1 ) and anabolic ( p 70 ( s6k ) and GSK 3beta ) targets in human skeletal muscle atrophy . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
By measuring Akt and S6K phosphorylation as a functional assay for TORC 1 and 2 , here , we report that dRheb has an inhibitory effect on dTORC 2 activity in Drosophila S 2 cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Upstream regulators of S6K , such as PDK 1 and protein kinase B ( PKB / Akt ) , are recruited to the membrane via their pleckstrin homology ( PH ) or protein protein interaction domains . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Current models suggest that AKT acts directly , or indirectly via the TSC complex , to activate the mammalian target of rapamycin ( mTOR ) as the main downstream mediator of AKT signaling . mTOR activation results in subsequent activation of S6K and STAT 3 , as well as suppression ( i . e . , phosphorylation ) of 4E BP 1 , leading to cell cycle progression and inhibition of apoptosis . ^^^ Within individual tumors , increased expression levels of p TSC 2 , p mTOR , p 4E BP 1 , p S6K , p S 6 , and p STAT 3 were found in regions defined by elevated AKT activation . ^^^ However , only TSC 2 , S6K , and S 6 activation levels correlated significantly with AKT activation and clustered together in multidimensional scaling analyses . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Emphasis will be put on three serine / threonine kinases , mTOR , Akt and S 6 Kinase ( S6K ) , and their role in the integration of environmental cues and the coordination of muscle growth . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Recent studies indicate that phosphatidylinositide 3OH kinase ( PI3K ) induced S 6 kinase ( S6K1 ) activation is mediated by protein kinase B ( PKB ) . ^^^ Here we set out to examine the importance of PKB signaling in S6K1 activation . ^^^ However , of these two mutants , only the constitutively membrane targeted allele of PKB induces S6K1 activation . ^^^ Furthermore , an interfering mutant of PKB , which blocks insulin induced PKB activation and GSK 3beta inactivation , has no effect on S6K1 activation . ^^^ The results demonstrate that PKB mediates S6K1 activation only as a function of constitutive membrane localization , whereas the activation of PKB appears both necessary and sufficient to induce 4E BP 1 phosphorylation independently of its intracellular location . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We report that S6K2 is activated similarly to S6K1 by the PI 3 K effectors phosphoinositide dependent kinase 1 , Cdc 42 , Rac , and protein kinase Czeta but that S6K2 is more sensitive to basal activation by myristoylated protein kinase Czeta than is S6K1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Upstream regulators of S6K1 and Akt include phosphoinositide 3 kinase ( PI 3 K ) and 3 phosphoinositide dependent kinase 1 ( PDK 1 ) . ^^^ Whereas TPCK had no effect on either mitogen regulated PI 3 K activity or total cellular PDK 1 activity , TPCK prevented phosphorylation of the PDK 1 regulatory sites in S6K1 and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
One component involved here is p 70 S6 kinase 1 ( S6K1 ) , which lies downstream of mammalian target of rapamycin , whose regulation is thought to involve phosphatidylinositol 3 kinase and protein kinase B ( PKB ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Overall , the results suggest that the blunted protein synthetic response observed in 26 vs . 7 day old neonatal pigs is due in part to decreased content and / or activity of signaling components downstream of PI 3 kinase , e . g . , PKB , mTOR , and S6K1 . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , Akt , another phosphatidylinositol 3 kinase effector and regulator of S6K1 , also increased Thr ( 389 ) phosphorylation in a S6K1 activity dependent manner . ^^^ We conclude that S6K1 activity is required for maximal Thr ( 389 ) phosphorylation by mitogens and by multiple phosphatidylinositol 3 kinase dependent inputs including PDK 1 , PKCzeta , and Akt , and we propose that autophosphorylation is an important regulatory mechanism for phosphorylation of the hydrophobic motif Thr ( 389 ) site in S6K1 . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We found a similar pattern in the regulation of Akt , a kinase upstream from S6K1 . ^^^ IRS 1 content and insulin responsiveness of PI3K , Akt , and S6K1 showed a transition to the adult phenotype during the first several postnatal weeks . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
This effect is associated with a reduction in the phosphorylation and activation of the serine threonine kinases Akt 1 and p 70 S6 kinase ( S6K1 ) , two downstream targets of phosphoinositide dependent kinase 1 ( PDK 1 ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , despite appropriate stimulation of IGF 1 receptor , IRS 1 and PKB , EtOH impairs IGF 1 signaling via S6K1 and 4E BP 1 pathways , and this defect is regulated in a glucocorticoid and TNF independent manner . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Increased clearance of mutant huntingtin by raised glucose ( 8 g / l ) and 2DOG correlated with increased autophagy and reduced phosphorylation of mTOR , S6K1 and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
By contrast , an inhibitor of epidermal growth factor receptor kinase , AG 1478 , which prevents carbachol stimulated ErbB 3 transactivation , PI3K recruitment and protein kinase B activation in 1321N1 cells , reduced activation of S6K1 by no more than 30 % . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Moreover , Rheb overexpression induces S6K1 phosphorylation and inhibits PKB phosphorylation , as do loss of function mutations in TSC1 / 2 , but contrary to earlier reports Rheb has no effect on MAPK phosphorylation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
To understand the role of arachidonic acid ( AA ) in regulating vascular smooth muscle cell ( VSMC ) growth , its effects on phosphorylation of Akt , S6K1 , ribosomal protein S 6 , 4EBP1 , and eIF4E were studied . ^^^ Arachidonic acid stimulated phosphorylation of Akt , S6K1 , ribosomal protein S 6 , 4EBP1 , and eIF4E in a time dependent manner in VSMC . ^^^ Metabolic conversion of AA via the LOX / MOX and / or COX pathways , to some extent , was required for its effects on the phosphorylation of Akt , S6K1 , ribosomal protein S 6 , 4EBP1 , and eIF4E . ^^^ LY 294002 , an inhibitor of PI3K , completely blocked AA induced phosphorylation of Akt , S6K1 , ribosomal protein S 6 , 4EBP1 , and eIF4E , suggesting a role for PI3K in these effects . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
A similar pattern for protein kinase B phosphorylation was observed , upstream from S6K1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , overexpression of S6K1 , and phosphorylated Akt independent of phosphatase and tensin homologue deleted from chromosome 10 status , were associated with rapamycin sensitivity . ^^^ Targeting S6K1 and Akt with small interfering RNA and dominant negative constructs , respectively , decreased rapamycin sensitivity . ^^^ CONCLUSIONS : Overexpression of S6K1 and expression of phosphorylated Akt should be evaluated as predictors of rapamycin sensitivity in breast cancer patients . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Incorporation of L [ 1 13C ] leucine in muscle proteins ( fractional synthesis rate , FSR ) was measured in vastus lateralis , before and during a euglycemic hyperinsulinemic hyperaminoacidemic clamp , together with Western blot analysis of protein kinase B ( PKB ) , mTOR , 4E BP 1 , and S6K1 phosphorylation . ^^^ Phosphorylation of PKB , mTOR , and 4E BP 1 were similarly increased by insulin and amino acid in both groups , except for S6K1 phosphorylation , which was not stimulated in elderly subjects . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Ectopic expression of active protein kinase B or active S6K1 abrogated the dual inhibitor mediated down regulation of cyclin D 1 expression , demonstrating the importance of these FGFR 4 / ErbB2 signaling targets in regulating cyclin D 1 translation . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
As in murine cells , rapamycin treatment of human adipocytes inhibited S6K1 , blunted Ser636 / 639 phosphorylation of IRS 1 , leading to increased Akt activation and glucose uptake by insulin . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Time course studies also revealed that mTOR and S6K1 activation by insulin was accelerated in tissues of obese rats , in association with increased inhibitory phosphorylation of insulin receptor substrate 1 ( IRS 1 ) on Ser636 / Ser639 and impaired Akt activation . ^^^ The relationship between mTOR / S6K1 overactivation and impaired insulin signaling to Akt was also examined in hepatic cells in vitro . ^^^ Inhibition of mTOR / S6K1 by rapamycin blunted insulin induced Ser636 / Ser639 phosphorylation of IRS 1 , leading to a rapid ( approximately 5 min ) and persistent increase in IRS 1 associated phosphatidylinositol 3 kinase activity and Akt phosphorylation . ^^^ In vitro studies with rapamycin suggest that mTOR / S6K1 overactivation contributes to elevated serine phosphorylation of IRS 1 , leading to impaired insulin signaling to Akt in liver and muscle of this dietary model of obesity . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Here we show that S 6 kinase 1 ( S6K1 ) , a protein kinase activated by nutrients and insulin like growth factors ( IGFs ) , is essential for the control of muscle cytoplasmic volume by Akt and mTOR . ^^^ In the differentiated state , S6K1 ( / ) myotubes have a normal number of nuclei but are smaller , and their hypertrophic response to IGF 1 , nutrients and membrane targeted Akt is blunted . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
There was also suppression in phosphorylated PKB Thr ( 308 ) , forkhead in rhabdomyosarcoma , S6K1 , S 6 , 4E BP 1 , and signal transducers and activators of transcription 3 Tyr ( 705 ) and Ser ( 727 ) protein levels with ILK inhibition by QLT 0254 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Activation of mTOR by FGF 9 induces p 70 ribosomal S 6 kinase ( S6K1 ) phosphorylation , cyclin expression , and cell proliferation , which are independent of phosphatidylinositol 3 kinase and Akt . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Nicotinic activation of Akt increased phosphorylation of multiple downstream substrates of Akt in a time dependent manner , including GSK 3 , FKHR , tuberin , mTOR and S6K1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In contrast , the ability of a maximally stimulating dose of insulin to increase the phosphorylation of PKB , 4E BP 1 , S6K1 , or mTOR was not altered 20 min after intravenous injection . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We show that S 6 kinase 1 ( S6K1 ) , but not Akt , directly phosphorylates mTOR in cell free in vitro system and in cells . ^^^ Expression of a constitutively active , rapamycin and wortmannin resistant S6K1 leads to constitutive phosphorylation of mTOR , whereas knock down of S6K1 using small inhibitory RNA greatly reduces mTOR phosphorylation despite elevated Akt activity . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Activation of the potential upstream regulators of 4E BP 1 and S6K1 phosphorylation via PKB and mTOR was also observed . ^^^ Furthermore , the results are consistent with a role for assembly of active eIF4G . eIF4E complex and activation of S6K1 in mediating the stimulation of mRNA translation initiation by IGF 1 through a PKB / mTOR signaling pathway . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Overexpression of hVps 34 or the associated hVps 15 kinase activates S6K1 , and insulin stimulation of S6K1 is blocked by microinjection of inhibitory anti hVps 34 antibodies , overexpression of a FYVE domain construct that sequesters the hVps 34 product PI3P , or small interfering RNA mediated knock down of hVps 34 . hVps 34 is not part of the insulin input to S6K1 , as it is not stimulated by insulin , and inhibition of hVps 34 has no effect on phosphorylation of Akt or TSC 2 in insulin stimulated cells . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
S ) hydroxyeicosatetraenoic acid induces angiogenesis via activation of PI3K Akt mTOR S6K1 signaling . ^^^ Because 15 ( S ) HETE was found to be more potent than 5 ( S ) HETE and 12 ( S ) HETE in HDMVEC tube formation , we next focused on elucidation of the signaling mechanisms underlying its angiogenic activity . 15 ( S ) HETE stimulated Akt and S6K1 phosphorylation in HDMVEC in a time dependent manner . ^^^ Wortmannin and LY 294002 , two specific inhibitors of phosphatidylinositol 3 kinase ( PI3K ) , blocked both Akt and S6K1 phosphorylation , whereas rapamycin , a specific inhibitor of Akt downstream effector , mammalian target of rapamycin ( mTOR ) , suppressed only S6K1 phosphorylation induced by 15 ( S ) HETE suggesting that this eicosanoid activates the PI3K Akt mTOR S6K1 signaling in HDMVEC . ^^^ Pharmacologic inhibition of PI3K Akt mTOR S6K1 signaling completely suppressed 15 ( S ) HETE induced in vivo angiogenesis . ^^^ Together , these results show for the first time that 15 ( S ) HETE stimulates angiogenesis via activation of PI3K Akt mTOR S6K1 signaling . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
However , only the EBV+ / III transformed B cells displayed also activation of the phosphatidylinositol 3 kinase ( PI3K ) / Akt pathway that is considered to be the key activator of mTOR and of the mitogen activated protein kinase / extracellular signal regulated kinase ( ERK ) kinase ( MEK ) / ERK pathway that coactivates one of the immediate targets of mTOR , p 70 S6K1 . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
To understand the mechanisms by which thrombin induces vascular smooth muscle cell ( VSMC ) DNA synthesis and motility , we have studied the role of phosphatidylinositol 3 kinase ( PI3K ) Akt mammalian target of rapamycin ( mTOR ) S6K1 signaling . ^^^ Thrombin stimulated the phosphorylation of Akt and S6K1 in VSMC in a sustained manner . ^^^ Blockade of PI3K Akt mTOR S6K1 signaling by LY 294002 , and rapamycin suppressed both thrombin induced VSMC DNA synthesis and migration . ^^^ In addition , thrombin stimulated the tyrosine phosphorylation of EGF receptor ( EGFR ) , and inhibition of its kinase activity significantly blocked Akt and S6K1 phosphorylation , Fra 1 and FGF 2 expression , DNA synthesis , and motility induced by thrombin in VSMC . ^^^ Together these observations suggest that thrombin induces both VSMC DNA synthesis and motility via EGFR dependent stimulation of PI3K / Akt signaling targeting in parallel the Fra 1 mediated FGF 2 expression and mTOR S6K1 activation . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
In the present study , we investigated the possible additional participation of a phosphatidylinositol 3 kinase ( PI3K ) / serine threonine protein kinase B ( Akt ) / mammalian target of rapamycin ( mTOR ) / p70 ribosomal S 6 kinase ( S6K1 ) pathway in this growth response . ^^^ We found transient activation of Akt ( Ser 473 ) and more prolonged activation of S6K1 by 5 HT . ^^^ Inhibition of Akt with NL 71 101 and downregulation of Akt expression with Akt small interfering RNA blocked 5 HT induced S6K1 phosphorylation . ^^^ We conclude from these studies that a parallel PI3K and reactive oxygen species dependent Akt / mTOR / S6K1 pathway participates independently from MAPK and Rho / ROCK in the mitogenic effect of 5 HT on pulmonary artery SMCs . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Recent studies have revealed that the signaling pathways regulating the mammalian target of rapamycin such as Akt and S6K1 are frequently activated in pancreatic cancer . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Because 14 , 15 EET was found to be slightly more efficacious than 5 , 6 , 8 , 9 , and 11 , 12 EETs in stimulating HDMVEC tube formation and migration , we next focused on elucidation of the signaling mechanisms underlying its angiogenic activity . 14 , 15 EET stimulated Akt and S6K1 phosphorylation in Src and phosphatidylinositol 3 kinase ( PI3K ) dependent manner in HDMVECs . ^^^ Together , these results show for the first time that Src and PI3K Akt signaling via targeting in parallel with FGF 2 expression and mTOR S6K1 activation plays an indispensable role in 14 , 15 EET induced angiogenesis . . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We found that the Akt , mTOR and p 70 S6 kinase ( S6K1 ) from the PI3K / mTOR signaling pathway were activated in all of the pancreatic cancer cell lines examined . ^^^ When surgically resected tissue specimens of pancreatic ductal adenocarcinoma were examined , phosphorylation of Akt , mTOR and S6K1 was detected in 50 , 55 and 65 % of the specimens , respectively . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
We also characterized insulin signaling pathways believed to promote myocyte growth and interact with proliferative responses mediated by G protein coupled receptors , and we assessed myocardial insulin receptor substrate 1 ( IRS 1 ) and p 110 alpha catalytic and p 85 regulatory subunits of phospatidylinositol 3 kinase ( PI3K ) , Akt , MEK , ERK1 / 2 , and S 6 kinase 1 ( S6K1 ) . ^^^ Insulin decreased AT1a R mRNA expression but increased protein levels and increased AT 2 R mRNA and protein levels and phosphorylation of IRS 1 ( Ser374 / Tyr989 ) , MEK1 / 2 ( Ser218 / Ser222 ) , ERK1 / 2 ( Thr202 / Tyr204 ) , S6K1 ( Thr421 / Ser424 / Thr389 ) , Akt ( Thr308 / Thr308 ) , and PI3K p 110 alpha but not of p 85 ( Tyr 508 ) . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Furthermore , the inhibition of PI3K Akt , but not ERK 1 / 2 pathway , attenuated M . tbc induced S6K1 phosphorylation , whereas PI3K inhibition enhanced p 38 phosphorylation and apoptosis signal regulating kinase 1 activity during exposure to M . tbc . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
The IRS 1 , PIK3R1 , PIK3R2 , AKT 2 , AKT 3 , FRAP 1 , and RPS6KB1 genes were neither amplified nor overexpressed in any of the tumors . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
Phosphorylation of AKT was stimulated by insulin only , while phosphorylation of MAPK3 / 1 and RPS6KB1 was increased by insulin and oxidative stress . ^^^
Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
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Interacting proteins: P23443 and P31749	Pubmed	SVM Score :0.0
NA