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- W2065402899 abstract "Tumor cells typically resist programmed cell death (apoptosis) induced by death receptors. Activated death receptors evoke Bax conformational change, cytochrome c release, and cell death. We report that the tumor suppressor gene RASSF1A is required for death receptor-induced Bax conformational change and apoptosis. TNFα or TRAIL stimulation induced recruitment of RASSF1A and MAP-1 to receptor complexes and promoted complex formation between RASSF1A and the BH3-like protein MAP-1. Normally, MAP-1 is inhibited by an intramolecular interaction. RASSF1A/MAP-1 binding relieved this inhibitory interaction, resulting in MAP-1 association with Bax. Deletion of the RASSF1A gene or short hairpin silencing of either RASSF1A or MAP-1 expression blocked MAP-1/Bax interaction, Bax conformational change and mitochondrial membrane insertion, cytochrome c release, and apoptosis in response to death receptors. Our findings identify RASSF1A and MAP-1 as important components between death receptors and the apoptotic machinery and reveal a potential link between tumor suppression and death receptor signaling." @default.
- W2065402899 created "2016-06-24" @default.
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- W2065402899 date "2005-06-01" @default.
- W2065402899 modified "2023-10-08" @default.
- W2065402899 title "The Tumor Suppressor RASSF1A and MAP-1 Link Death Receptor Signaling to Bax Conformational Change and Cell Death" @default.
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- W2065402899 doi "https://doi.org/10.1016/j.molcel.2005.05.010" @default.
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