| Identifier | HPI102999 |
| Interaction | p27 <==> p53 |
| Role & State | RS:0000080,suppressor; |
| Interaction Type | IT:0000176,suppress; IT:0000080,effect; IT:0000078,regulation; |
| Biological Process | BP:0007050,cell cycle arrest; BP:0010467,gene expression; BP:0051320,S phase; BP:0007049,cell cycle; BP:0006915,apoptosis; BP:0040007,growth; |
| Biological Function | --- |
| Subcelluar Location | --- |
| Detection Method | --- |
| Reference | 10773877_12, In contrast to the dramatic effects of p27-deficiency on hGHRH-induced organ growth, elimination of p53, by crossbreeding MT-hGHRH mice to p53-deficient mice, did not augment the hyperplastic/tumorigenic effects of hGHRH transgene expression.
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| Reference | 18373075_5, However, at a low dose of etoposide (repairable damage), Bid activated the S phase checkpoint through the up-regulation of p21 and p27, which are both p53-independent.
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| Reference | 19528460_2, In our previous study, the recombinant adenovirus expressing wild-type p27(kip1) (Adp27-wt) induced cell cycle arrest and apoptosis, and proved that p27 is a tumor suppressor gene like p53.
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| Reference | 19672859_9, The enhanced survival of patients with well differentiated compared to poorly-differentiated tumors was related to high expression of p27, p21 and p53 in liver sections.
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