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- W2116145077 abstract "Recent efforts to develop pharmacologic agents that restore function to mutant forms of p53 hold significant promise in cancer therapy. Here, we examine the effects of such pharmacologic activation of p53 function using a small molecule, PRIMA-1, and a model system employing a p53 protein fused to a mutant steroid binding domain of the murine estrogen receptor (p53ERtam) that renders it responsive only in the presence of 4-hydroxytamoxifen. In either case, p53 activation triggered apoptosis that was not inhibited by the presence of macromolecular synthesis inhibitors. This p53-induced, transcription-independent apoptosis is Bax dependent, proceeds in the absence of a nucleus, and involves Bax translocation and cytochrome c release. Hence, pharmacologic p53 modulators can activate a transcription-independent apoptotic program." @default.
- W2116145077 created "2016-06-24" @default.
- W2116145077 creator A5016580341 @default.
- W2116145077 creator A5036507802 @default.
- W2116145077 creator A5056776085 @default.
- W2116145077 creator A5075655484 @default.
- W2116145077 date "2003-11-01" @default.
- W2116145077 modified "2023-10-17" @default.
- W2116145077 title "Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription" @default.
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- W2116145077 doi "https://doi.org/10.1016/s1535-6108(03)00272-1" @default.
- W2116145077 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14667504" @default.
- W2116145077 hasPublicationYear "2003" @default.
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