Jun and JNK kinase are activated in thymocytes in response to VM26 and radiation but not glucocorticoids

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DOIResolve DOI: http://doi.org/10.1006/excr.1996.3419
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TypeArticle
Journal titleExperimental Cell Research
Volume230
Issue2
Pages220232; # of pages: 13
AbstractIn order to establish what role members of the activating protein-1 (AP-1) gene families, i.e., c-fos,c-jun, junB,andjunD,play in thymic apoptosis, we have analyzed changes in their expression in response to three different agents: a glucocorticoid analog dexamethasone, an inhibitor of topoisomerase II teniposide VM26, and gamma radiation. All three agents induced thymic death at a similar rate and with the same morphological and biochemical features. There was a rapid and transient increase in the steady-state mRNA level ofjunBand c-fosgenes in all treatments, including control cultures, reminiscent rather of cellular stress response to the environmental changes than to the apoptotic stimuli. On the other hand, treatments with the DNA-damaging agents, VM26 and gamma radiation, resulted in superinduction of the c-junmRNA and in the activation of the stress response signaling pathway of c-Jun N-terminal kinase. Gene transcription ceased completely in cells with fragmented DNA and the down-regulation of genes such asjunDandtubulinwas reflective of the thymocytes’ commitment to apoptosis. The DNA-binding activities of the serum response factors, cyclic AMP response element binding proteins, and AP-1 factors, indicative of their transcriptional competence, were compromised shortly after induction of apoptosis regardless of the agent employed, consistent with previously reported enhancement in cellular proteolysis which is an essential component of the apoptotic cell death.
Publication date
LanguageEnglish
AffiliationNRC Institute for Biological Sciences; National Research Council Canada
Peer reviewedNo
NRC numberTESTOLIN1997
TESTOLIN1997A
NPARC number9374296
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Record identifierded15ee1-7833-4489-bf77-4068e6faa02b
Record created2009-07-10
Record modified2016-06-01
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