| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| Activated Notch 1 inhibits p 53 induced apoptosis and sustains transformation by human papillomavirus type 16 E 6 and E 7 oncogenes through a PI3K PKB / Akt dependent pathway . ^^^ |
|
| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| We present evidence that endogenous Notch 1 associates with p 56 ( lck ) and PI3K but that Akt / PKB does not co immunoprecipitate with the Notch1 . p56 ( lck ) . ^^^ |
|
| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| Inhibition of endothelial cell proliferation by Notch 1 signaling is mediated by repressing MAPK and PI3K / Akt pathways and requires MAML 1 . ^^^ Following Notch 1 activation , both pathways were suppressed in endothelial cells , and alterations in MAPK or PI3K / Akt pathway activity reversed Notch 1 induced growth inhibition . ^^^ Overexpression of a dominant negative mutant of MAML 1 antagonized the effects of activated Notch 1 on the MAPK and PI3K / Akt pathways . ^^^ |
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| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| Inhibition of either the MAPK or the phosphatidylinositol 3 kinase ( PI3K ) Akt pathway reverses the Notch 1 signaling induced tumor cell growth . ^^^ |
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| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| Finally , we show that MCF 7 ( breast cancer ) and MOLT 4 ( T cell acute lymphoblastic leukemia ) cells having aberrant Notch 1 signaling are chemoresistant , which can be reversed by both PI3K and mTOR inhibitors . ^^^ These results establish that Notch 1 signaling confers chemoresistance by inhibiting p 53 pathway through mTOR dependent PI3K Akt / PKB pathway and imply that p 53 status perhaps is an important determinant in combination therapeutic strategies , which use mTOR inhibitors and chemotherapy . . ^^^ |
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| Interacting proteins: P48736 and P46531 |
Pubmed |
SVM Score :0.0 |
| NA |
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