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001-es BibID:	bibEBI12985
Első szerző:	Wikonkál Norbert, M.
Cím:	Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice / Wikonkal, N. M., Remenyik, É., Knezevich, D., Zhang, W., Liu, M., Zhao, H., Berton, T. R., Johnson, D. G., Brash, D. E.
Dátum:	2003
Megjegyzések:	The E2f1 transcription factor, which regulates genes required for S-phase entry, also induces apoptosis by transcriptional and post-translational mechanisms. As E2f1 is inducible by DNA damage we investigated its importance in vivo in ultraviolet (UV)-induced apoptosis, a protective mechanism that prevents the epidermis from accumulating UV-induced mutations. Contrary to expectation, E2f1-/- mice demonstrated enhanced keratinocyte apoptosis after UVB exposure, whereas apoptosis was suppressed by epidermis-specific overexpression of human E2F1. Apoptosis induced by -radiation was also repressed by E2f1. E2f1-/-;Trp53-/- double knockout mice exhibited the elevated UVB-induced apoptosis of E2f1-/- alone, rather than the profound apoptosis defect seen in Trp53-/- mice, indicating that Trp53 (p53) lies functionally upstream of E2f1. Transfecting E2F1 into E2f1-/-;Trp53-/- primary fibroblasts suppressed UVB-induced apoptosis and this suppression was relieved by Trp53. The double knockout also reverted the abnormal sex ratio and early-onset tumours of Trp53-/- mice. These results imply that E2f1 functions as a suppressor of an apoptosis pathway that is initiated by DNA photoproducts and perhaps genetic abnormalities; p53 relieves this suppression.
Tárgyszavak:	idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Nature Cell Biology. - 5 : 7 (2003), p. 655-660. -
További szerzők:	Remenyik Éva (1956-) (bőrgyógyász) Knezevich, Dejan Zhang, Wengeng Liu, Ming Zhao, Hongyu Berton, T. R. Johnson, David G. Brash, Douglas E.
Internet cím:	DOI
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