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- W2000823493 abstract "In mammals, one of the key regulators necessary for responding to genotoxic stress is the p53 transcription factor. p53 is the single most commonly mutated tumor suppressor gene in human cancers [1Hussain S.P. Harris C.C. Molecular epidemiology and carcinogenesis endogenous and exogenous carcinogens.Mutat Res. 2000; 462: 311-322Crossref PubMed Scopus (97) Google Scholar]. Here we report the identification of a C. elegans homolog of mammalian p53. Using RNAi and DNA cosuppression technology, we show that C. elegans p53 (cep-1) is required for DNA damage-induced apoptosis in the C. elegans germline. However,cep-1 RNAi does not affect programmed cell death occurring during worm development and physiological (radiation-independent) germ cell death. The DNA binding domain of CEP-1 is related to vertebrate p53 members and possesses the conserved residues most frequently mutated in human tumors. Consistent with this, CEP-1 acts as a transcription factor and is able to activate a transcriptional reporter containing consensus human p53 binding sites. Our data support the notion that p53-mediated transcriptional regulation is part of an ancestral pathway mediating DNA damage-induced apoptosis and reveals C. elegans as a genetically tractable model organism for studying the p53 apoptotic pathway." @default.
- W2000823493 created "2016-06-24" @default.
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- W2000823493 date "2001-10-01" @default.
- W2000823493 modified "2023-10-11" @default.
- W2000823493 title "The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis" @default.
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- W2000823493 doi "https://doi.org/10.1016/s0960-9822(01)00534-6" @default.
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