Linked Life Data

12881712

Source:http://linkedlifedata.com/resource/pubmed/id/12881712

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pubmed-article:12881712pubmed:abstractTextForkhead family transcription factors are critical regulators of cell cycle progression and apoptosis in hematopoietic cells. Here, we show that FOXO3a (also known as FKHRL1) is a new substrate of caspase-3-like proteases during apoptosis in T lymphocytes. FOXO3a was cleaved in vivo by caspases in leukemic Jurkat cells following engagement of Fas (CD95) receptor, staurosporine, and etoposide treatment, but not following engagement of CD99, a caspase-independent cell death inducer. Caspase-mediated cleavage of FOXO3a was also observed in CD4+ peripheral T cells subjected to activation-induced cell death. The expression of the death adapter FADD and caspase-8 was required for Fas-induced FOXO3a cleavage, but activation of survival pathways by overexpression of FLICE-inhibitory protein or phorbol myristate acetate treatment prevented it. FOXO3a was cleaved in vitro by caspase-3-like proteases at the consensus sequence DELD304A, releasing the N-terminal DNA-binding domain of FOXO3a from its C-terminal transactivating domain. Whereas full-length FOXO3a enhanced Forkhead response element-dependent transcription and apoptosis in Jurkat cells, both fragments were inactive to promote gene activation and cell death. In contrast, a caspase-resistant FOXO3a mutant exhibited enhanced transcriptional and proapoptotic activities. Together, these results indicate that the proteolytic cleavage of FOXO3a by caspases may represent a novel regulatory mechanism of FOXO3a activity during death receptors signaling.lld:pubmed
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pubmed-article:12881712pubmed:articleTitleProteolytic regulation of Forkhead transcription factor FOXO3a by caspase-3-like proteases.lld:pubmed
pubmed-article:12881712pubmed:affiliationINSERM U343, IFR50, Hôpital de l'Archet, 06202 Nice, France.lld:pubmed
pubmed-article:12881712pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12881712pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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