| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| No differences in the pattern of TP 53 and K ras mutations were detected between post HD and sporadic cancers . ^^^ |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| Since its discovery in 1996 , SUMO has received a high degree of attention because of its intriguing and essential functions , and because its substrates include a variety of biomedically important proteins such as tumor suppressor p 53 , c jun , PML and huntingtin . ^^^ |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : TP 53 is an attractive candidate for modifying age of onset ( AO ) in Huntington disease ( HD ) : The amino terminus of the mutated huntingtin ( htt ) exon 1 translation product has functional properties which may affect critically the TP 53 pathway in HD neurons . ^^^ |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| To clarify whether host genetic factors contribute to secondary tumorigenesis , we performed mutational analyses of the TP 53 , BRCA 1 , and BRCA 2 tumor suppressor genes in a cohort of 44 HD patients developing one or more SMN . ^^^ CONCLUSION : Despite features suggestive of genetic predisposition , the TP 53 , BRCA 1 , and BRCA 2 genes were not frequently mutated in this cohort of HD patients developing SMNs . ^^^ |
|
| Interacting proteins: P42858 and P04637 |
Pubmed |
SVM Score :0.0 |
| In the present investigation , we studied two single nucleotide polymorphisms ( SNPs ) , namely , R72P in TP 53 gene coding for transcription factor p 53 , which interacts with Htt protein and R196K in human caspase activated DNase ( hCAD ) gene involved in apoptosis to investigate their role as genetic modifiers of the AO of HD . ^^^ Multiple linear regression analysis revealed that variations in TP 53 and hCAD genes explained 12 . 6 % and 6 % , respectively , of the variance in the AO of HD after accounting for the effect of expanded CAG repeats . ^^^ This data demonstrated that variations in TP 53 and hCAD genes modulate the AO of HD . . ^^^ |
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