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Article: FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis

TitleFADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
Authors
Issue Date1998
Citation
Science, 1998, v. 279, n. 5358, p. 1954-1958 How to Cite?
AbstractFADD (also known as Mort-1) is a signal transducer downstream of cell death receptor opes (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR1), and death receptor 3 (DR3) did not induce apoptosis in FADD- deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemoterapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproductive the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.
Persistent Identifierhttp://hdl.handle.net/10722/291931
ISSN
2023 Impact Factor: 44.7
2023 SCImago Journal Rankings: 11.902
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYeh, Wen Chen-
dc.contributor.authorDe La Pompa, José Luis-
dc.contributor.authorMcCurrach, Mila E.-
dc.contributor.authorShu, Hong Bing-
dc.contributor.authorElia, Andrew J.-
dc.contributor.authorShahinian, Arda-
dc.contributor.authorNg, Michelle-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorKhoo, Wilson-
dc.contributor.authorMitchell, Kyran-
dc.contributor.authorEl-Deiry, Wafik S.-
dc.contributor.authorLowe, Scott W.-
dc.contributor.authorGoeddel, David V.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:25Z-
dc.date.available2020-11-17T14:55:25Z-
dc.date.issued1998-
dc.identifier.citationScience, 1998, v. 279, n. 5358, p. 1954-1958-
dc.identifier.issn0036-8075-
dc.identifier.urihttp://hdl.handle.net/10722/291931-
dc.description.abstractFADD (also known as Mort-1) is a signal transducer downstream of cell death receptor opes (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR1), and death receptor 3 (DR3) did not induce apoptosis in FADD- deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemoterapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproductive the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.-
dc.languageeng-
dc.relation.ispartofScience-
dc.titleFADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1126/science.279.5358.1954-
dc.identifier.pmid9506948-
dc.identifier.scopuseid_2-s2.0-7144263731-
dc.identifier.volume279-
dc.identifier.issue5358-
dc.identifier.spage1954-
dc.identifier.epage1958-
dc.identifier.isiWOS:000072613300051-
dc.identifier.issnl0036-8075-

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