File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Stress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3

TitleStress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3
Authors
Issue Date1997
Citation
Nature, 1997, v. 385, n. 6614, p. 350-352 How to Cite?
AbstractDistinct and evolutionarily conserved signal transduction cascades mediate survival or death in response to developmental and environmental cues. The stress-activated protein kinases, or Jun N-terminal kinases (SAPKs/JNKs), are activated in response to a variety of cellular stresses such as changes in osmolarity and metabolism, DNA damage, heat shock, ischaemia, or inflammatory cytokines. Sek1 (JNKK/MKK4) is a direct activator of SAPKs/JNKs in response to environmental stresses or mitogenic factors. Here we investigate the role of Sek1 in development and apoptosis by deleting sek1 in embryonic stem (ES) cells by homologous recombination. We provide genetic evidence that different stresses utilize distinct signalling pathways for SAPK/JNK activation. sek1(-/-)/rag2(-/-) chimaeric mice have normal numbers of mature T cells but fewer immature CD4+CD8+ thymocytes. The sek1 mutation did not affect the induction of apoptosis in response to environmental stresses in ES and T cells: instead, sek1 protected thymocytes from CD95 (Fas)- and CD3-mediated apoptosis. These data indicate that SEK1 mediates survival signals in T-cell development.
Persistent Identifierhttp://hdl.handle.net/10722/291346
ISSN
2020 Impact Factor: 49.962
2020 SCImago Journal Rankings: 15.993
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNishina, Hiroshi-
dc.contributor.authorFischer, Klaus D.-
dc.contributor.authorRadvanyi, Laszlo-
dc.contributor.authorShahinian, Arda-
dc.contributor.authorHakem, Razqallah-
dc.contributor.authorRubie, Elizabeth A.-
dc.contributor.authorBernstein, Alan-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorWoodgett, James R.-
dc.contributor.authorPenninger, Josef M.-
dc.date.accessioned2020-11-17T14:54:10Z-
dc.date.available2020-11-17T14:54:10Z-
dc.date.issued1997-
dc.identifier.citationNature, 1997, v. 385, n. 6614, p. 350-352-
dc.identifier.issn0028-0836-
dc.identifier.urihttp://hdl.handle.net/10722/291346-
dc.description.abstractDistinct and evolutionarily conserved signal transduction cascades mediate survival or death in response to developmental and environmental cues. The stress-activated protein kinases, or Jun N-terminal kinases (SAPKs/JNKs), are activated in response to a variety of cellular stresses such as changes in osmolarity and metabolism, DNA damage, heat shock, ischaemia, or inflammatory cytokines. Sek1 (JNKK/MKK4) is a direct activator of SAPKs/JNKs in response to environmental stresses or mitogenic factors. Here we investigate the role of Sek1 in development and apoptosis by deleting sek1 in embryonic stem (ES) cells by homologous recombination. We provide genetic evidence that different stresses utilize distinct signalling pathways for SAPK/JNK activation. sek1(-/-)/rag2(-/-) chimaeric mice have normal numbers of mature T cells but fewer immature CD4+CD8+ thymocytes. The sek1 mutation did not affect the induction of apoptosis in response to environmental stresses in ES and T cells: instead, sek1 protected thymocytes from CD95 (Fas)- and CD3-mediated apoptosis. These data indicate that SEK1 mediates survival signals in T-cell development.-
dc.languageeng-
dc.relation.ispartofNature-
dc.titleStress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/385350a0-
dc.identifier.pmid9002521-
dc.identifier.scopuseid_2-s2.0-0031029214-
dc.identifier.volume385-
dc.identifier.issue6614-
dc.identifier.spage350-
dc.identifier.epage352-
dc.identifier.isiWOS:A1997WD91400053-
dc.identifier.issnl0028-0836-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats