Reactive oxygen species mediate crosstalk between NF-κB and JNK
The activation of NF- κ B inhibits apoptosis via a mechanism involving upregulation of various antiapoptotic genes, such as cellular FLICE-inhibitory protein (c-FLIP), Bcl-x L , A1/Bfl-1 , and X chromosome-liked inhibitor of apoptosis (XIAP). In contrast, the activation of c-Jun N-terminal kinase (J...
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Veröffentlicht in: | Cell death and differentiation 2006-05, Vol.13 (5), p.730-737 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | The activation of NF-
κ
B inhibits apoptosis via a mechanism involving upregulation of various antiapoptotic genes, such as
cellular FLICE-inhibitory protein (c-FLIP), Bcl-x
L
, A1/Bfl-1
, and
X chromosome-liked inhibitor of apoptosis (XIAP).
In contrast, the activation of c-Jun N-terminal kinase (JNK) promotes apoptosis in a manner that is dependent on the cell type and the context of the stimulus. Recent studies have indicated that one of the antiapoptotic functions of NF-
κ
B is to downregulate JNK activation. Further studies have also revealed that NF-
κ
B inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). In this review, we will focus on the signaling crosstalk between the NF-
κ
B and JNK cascades via ROS. |
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ISSN: | 1350-9047 1476-5403 |
DOI: | 10.1038/sj.cdd.4401830 |