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Article: Early lethality, functional NF-κB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice

TitleEarly lethality, functional NF-κB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice
Authors
Issue Date1997
Citation
Immunity, 1997, v. 7, n. 5, p. 715-725 How to Cite?
AbstractTRAF2 is an intracellular signal-transducing protein recruited to the TNFR1 and TNFR2 receptors following TNF stimulation. To investigate the physiological role of TRAF2, we generated TRAF2-deficient mice. traf2(-/-) mice appeared normal at birth but became progressively runted and died prematurely. Atrophy of the thymus and spleen and depletion of B cell precursors also were observed. Thymocytes and other hematopoietic progenitors were highly sensitive to TNF-induced cell death and serum TNF levels were elevated in these TRAF2-deficient animals. Examination of traf2(-/-) cells revealed a severe reduction in TNF-mediated JNK/SAPK activation but a mild effect on NF-κB activation. These results suggest that TRAF2-independent pathways of NF-κB activation exist and that TRAF2 is required for an NF- κB-independent signal that protects against TNF-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/292175
ISSN
2023 Impact Factor: 25.5
2023 SCImago Journal Rankings: 13.578
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYeh, Wen Chen-
dc.contributor.authorShahinian, Arda-
dc.contributor.authorSpeiser, Daniel-
dc.contributor.authorKraunus, Janine-
dc.contributor.authorBillia, Filio-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorDe La Pompa, José Luis-
dc.contributor.authorFerrick, David-
dc.contributor.authorHum, Betty-
dc.contributor.authorIscove, Norman-
dc.contributor.authorOhashi, Pamela-
dc.contributor.authorRothe, Mike-
dc.contributor.authorGoeddel, David V.-
dc.contributor.authorMak, Tak Wah-
dc.date.accessioned2020-11-17T14:55:55Z-
dc.date.available2020-11-17T14:55:55Z-
dc.date.issued1997-
dc.identifier.citationImmunity, 1997, v. 7, n. 5, p. 715-725-
dc.identifier.issn1074-7613-
dc.identifier.urihttp://hdl.handle.net/10722/292175-
dc.description.abstractTRAF2 is an intracellular signal-transducing protein recruited to the TNFR1 and TNFR2 receptors following TNF stimulation. To investigate the physiological role of TRAF2, we generated TRAF2-deficient mice. traf2(-/-) mice appeared normal at birth but became progressively runted and died prematurely. Atrophy of the thymus and spleen and depletion of B cell precursors also were observed. Thymocytes and other hematopoietic progenitors were highly sensitive to TNF-induced cell death and serum TNF levels were elevated in these TRAF2-deficient animals. Examination of traf2(-/-) cells revealed a severe reduction in TNF-mediated JNK/SAPK activation but a mild effect on NF-κB activation. These results suggest that TRAF2-independent pathways of NF-κB activation exist and that TRAF2 is required for an NF- κB-independent signal that protects against TNF-induced apoptosis.-
dc.languageeng-
dc.relation.ispartofImmunity-
dc.titleEarly lethality, functional NF-κB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/S1074-7613(00)80391-X-
dc.identifier.pmid9390694-
dc.identifier.scopuseid_2-s2.0-0031463025-
dc.identifier.volume7-
dc.identifier.issue5-
dc.identifier.spage715-
dc.identifier.epage725-
dc.identifier.isiWOS:A1997YH55400013-
dc.identifier.issnl1074-7613-

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