期刊
GENES & DEVELOPMENT
卷 18, 期 5, 页码 584-594出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1168104
关键词
MAPKKK; signal transduction; rel protein; proteosome; Imd
资金
- NCI NIH HHS [R01 CA076188, CA76188] Funding Source: Medline
- NIAID NIH HHS [AI43477, R01 AI043477, R37 AI043477] Funding Source: Medline
- NIGMS NIH HHS [GM50545, R01 GM050545] Funding Source: Medline
The molecular circuitry underlying innate immunity is constructed of multiple, evolutionarily conserved signaling modules with distinct regulatory targets. The MAP kinases and the IKK-NF-B-K molecules play important roles in the initiation of immune effector responses. We have found that the Drosophila NF-B-K protein Relish plays a crucial role in limiting the duration of INK activation and output in response to Gram-negative infections. Relish activation is linked to proteasomal degradation of TAK1, the upstream MAP kinase kinase kinase required for INK activation. Degradation of TAK1 leads to a rapid termination of INK signaling, resulting in a transient JNK-dependent response that precedes the sustained induction of Relish-dependent innate immune loci. Because the IKK-NF-KB module also negatively regulates INK activation in mammals, thereby controlling inflammation-induced apoptosis, the regulatory cross-talk between the INK and NF-KB pathways appears to be broadly conserved.
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