Stress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-01

AUTHORS

Hiroshi Nishina, Klaus D. Fischer, Laszlo Radvanyi, Arda Shahinian, Razqallah Hakem, Elizabeth A. Rubie, Alan Bernstein, Tak W. Mak, James R. Woodgett, Josef M. Penninger

ABSTRACT

Distinct 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)1,2, are activated in response to a variety of cellular stresses such as changes in osmolarity and metabolism, DNA damage, heat shock, ischaemia, or inflammatory cytokines3–6. Sek1 (JNKK/MKK4) is a direct activator of SAPKs/JNKs in response to environmental stresses or mitogenic factors7–9. 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. More... »

PAGES

350-353

Journal

TITLE

Nature

ISSUE

6614

VOLUME

385

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/385350a0

DOI

http://dx.doi.org/10.1038/385350a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045861763

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9002521


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59 cellular stress
60 changes
61 chimaeric mice
62 cues
63 damage
64 data
65 death
66 development
67 different stresses
68 direct activator
69 embryonic stem cells
70 environmental cues
71 environmental stress
72 evidence
73 genetic evidence
74 heat shock
75 homologous recombination
76 immature
77 induction
78 induction of apoptosis
79 ischaemia
80 kinase
81 mature T cells
82 metabolism
83 mice
84 mutations
85 normal numbers
86 number
87 osmolarity
88 pathway
89 protein kinase
90 recombination
91 response
92 role
93 shock
94 signal transduction
95 signals
96 stem cells
97 stress
98 stress-activated protein kinase
99 survival
100 survival signals
101 thymocytes
102 transduction
103 variety
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