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- Publisher Website: 10.1126/science.279.5358.1954
- Scopus: eid_2-s2.0-7144263731
- PMID: 9506948
- WOS: WOS:000072613300051
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Article: FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
Title | FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis |
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Authors | |
Issue Date | 1998 |
Citation | Science, 1998, v. 279, n. 5358, p. 1954-1958 How to Cite? |
Abstract | FADD (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 Identifier | http://hdl.handle.net/10722/291931 |
ISSN | 2023 Impact Factor: 44.7 2023 SCImago Journal Rankings: 11.902 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Yeh, Wen Chen | - |
dc.contributor.author | De La Pompa, José Luis | - |
dc.contributor.author | McCurrach, Mila E. | - |
dc.contributor.author | Shu, Hong Bing | - |
dc.contributor.author | Elia, Andrew J. | - |
dc.contributor.author | Shahinian, Arda | - |
dc.contributor.author | Ng, Michelle | - |
dc.contributor.author | Wakeham, Andrew | - |
dc.contributor.author | Khoo, Wilson | - |
dc.contributor.author | Mitchell, Kyran | - |
dc.contributor.author | El-Deiry, Wafik S. | - |
dc.contributor.author | Lowe, Scott W. | - |
dc.contributor.author | Goeddel, David V. | - |
dc.contributor.author | Mak, Tak W. | - |
dc.date.accessioned | 2020-11-17T14:55:25Z | - |
dc.date.available | 2020-11-17T14:55:25Z | - |
dc.date.issued | 1998 | - |
dc.identifier.citation | Science, 1998, v. 279, n. 5358, p. 1954-1958 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291931 | - |
dc.description.abstract | FADD (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.language | eng | - |
dc.relation.ispartof | Science | - |
dc.title | FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1126/science.279.5358.1954 | - |
dc.identifier.pmid | 9506948 | - |
dc.identifier.scopus | eid_2-s2.0-7144263731 | - |
dc.identifier.volume | 279 | - |
dc.identifier.issue | 5358 | - |
dc.identifier.spage | 1954 | - |
dc.identifier.epage | 1958 | - |
dc.identifier.isi | WOS:000072613300051 | - |
dc.identifier.issnl | 0036-8075 | - |