| First Author | Shimazaki K | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 422 |
| Issue | 1 | Pages | 133-8 |
| PubMed ID | 22564744 | Mgi Jnum | J:184516 |
| Mgi Id | MGI:5424272 | Doi | 10.1016/j.bbrc.2012.04.121 |
| Citation | Shimazaki K, et al. (2012) p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts. Biochem Biophys Res Commun 422(1):133-8 |
| abstractText | We studied the effects of Pin1, a regulatory molecule of the oncosuppressor p53, on both cell cycle arrest and apoptosis by treating primary mouse embryonic fibroblasts (MEFs) with etoposide. Etoposide induced G1 arrest in both wild-type and Pin1 null (pin1(-/-)) MEFs, and G2/M arrest and apoptotic cell death in MEFs lacking either p53 only (p53(-/-)) or both Pin1 and p53 (pin1(-/-)p53(-/-)). Both pin1(-/-) and pin1(-/-)p53(-/-) MEFs were enhanced the release of cytochrome c from the mitochondria, which might induce apoptosis. In response to etoposide treatment, apoptotic cell death was displayed in pin1(-/-)p53(-/-) MEFs but not in pin1(-/-) MEFs. These results suggest that p53 retards growth and suppresses etoposide-induced apoptosis in pin1(-/-) MEFs. |
