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Reactive oxygen special (ROS), troublemakers between nuclear factor-kB (NF-kB) and c-Jun NH2-terminal kinase (JNK).

Authors
Zhang-Y; Chen-F
Source
Cancer Res 2004 Mar; 64(6):1902-1905
NIOSHTIC No.
20025857
Abstract
Nuclear factor-kappaB (NF-kappaB) and c-Jun NH(2)-terminal kinase (JNK) are activated simultaneously under a variety of stress conditions. They also share several common signaling pathways for their activation in response to cytokines or growth factors. Recent studies, however, demonstrated a new form of interplay between these two allies. Inhibition of NF-kappaB by ikkbeta or rela gene deficiency sensitizes stress responses through enhanced or prolonged activation of JNK. Conversely, sustained activation of NF-kappaB inhibits cytokine-induced JNK activation. The mechanisms of how NF-kappaB and JNK become rivals for each other are under extensive debate.
Keywords
Growth-factors; Stress; Free-radicals
CODEN
CNREA8
Publication Date
20040315
Document Type
Journal Article
Email Address
lfd3@cdc.gov
Fiscal Year
2004
NTIS Accession No.
NTIS Price
Issue of Publication
6
ISSN
0008-5472
NIOSH Division
HELD
Source Name
Cancer Research
State
WV
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