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Article: Apaf1 is required for mitochondrial pathways of apoptosis and brain development

TitleApaf1 is required for mitochondrial pathways of apoptosis and brain development
Authors
Issue Date1998
Citation
Cell, 1998, v. 94, n. 6, p. 739-750 How to Cite?
AbstractApoptosis is essential for the precise regulation of cellular homeostasis and development. The role in vivo of Apaf1, a mammalian homolog of C. elegans CED-4, was investigated in gene-targeted Apaf1(-/-) mice. Apaf1-deficient mice exhibited reduced apoptosis in the brain and striking craniofacial abnormalities with hyperproliferation of neuronal cells. Apaf1- deficient cells were resistant to a variety of apoptotic stimuli, and the processing of Caspases 2, 3, and 8 was impaired. However, both Apaf1(-/-) thymocytes and activated T lymphocytes were sensitive to Fas-induced killing, showing that Fas-mediated apoptosis in these cells is independent of Apaf1. These data indicate that Apaf1 plays a central role in the common events of mitochondria-dependent apoptosis in most death pathways and that this role is critical for normal development.
Persistent Identifierhttp://hdl.handle.net/10722/291466
ISSN
2023 Impact Factor: 45.5
2023 SCImago Journal Rankings: 24.342
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYoshida, Hiroki-
dc.contributor.authorKong, Young Yun-
dc.contributor.authorYoshida, Ritsuko-
dc.contributor.authorElia, Andrew J.-
dc.contributor.authorHakem, Anne-
dc.contributor.authorHakem, Razqallah-
dc.contributor.authorPenninger, Josef M.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:26Z-
dc.date.available2020-11-17T14:54:26Z-
dc.date.issued1998-
dc.identifier.citationCell, 1998, v. 94, n. 6, p. 739-750-
dc.identifier.issn0092-8674-
dc.identifier.urihttp://hdl.handle.net/10722/291466-
dc.description.abstractApoptosis is essential for the precise regulation of cellular homeostasis and development. The role in vivo of Apaf1, a mammalian homolog of C. elegans CED-4, was investigated in gene-targeted Apaf1(-/-) mice. Apaf1-deficient mice exhibited reduced apoptosis in the brain and striking craniofacial abnormalities with hyperproliferation of neuronal cells. Apaf1- deficient cells were resistant to a variety of apoptotic stimuli, and the processing of Caspases 2, 3, and 8 was impaired. However, both Apaf1(-/-) thymocytes and activated T lymphocytes were sensitive to Fas-induced killing, showing that Fas-mediated apoptosis in these cells is independent of Apaf1. These data indicate that Apaf1 plays a central role in the common events of mitochondria-dependent apoptosis in most death pathways and that this role is critical for normal development.-
dc.languageeng-
dc.relation.ispartofCell-
dc.titleApaf1 is required for mitochondrial pathways of apoptosis and brain development-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/S0092-8674(00)81733-X-
dc.identifier.pmid9753321-
dc.identifier.scopuseid_2-s2.0-0032544564-
dc.identifier.volume94-
dc.identifier.issue6-
dc.identifier.spage739-
dc.identifier.epage750-
dc.identifier.isiWOS:000076021200007-
dc.identifier.f1000718691597-
dc.identifier.issnl0092-8674-

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