Journal
CELLULAR SIGNALLING
Volume 19, Issue 7, Pages 1372-1382Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2007.03.013
Keywords
negative regulator; feedback control; dephosphorylation; innate immunity; inflammation; cytokine; infection; MAP kinase
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Funding
- NIAID NIH HHS [R01 AI057798-03, R21 AI057798, R01 AI057798-01A1, R01 AI057798-04, R21 AI057798-01, AI 57798, R01 AI057798, R01 AI057798-02] Funding Source: Medline
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Mitogen-activated protein (MAP) kinase cascades are signal transduction pathways that play pivotal regulatory roles in the biosynthesis of proinflammatory cyrokines. MAP kinase phosphatase (MKP)-1, an archetypal member of the MKP family, is essential for the dephosphorylation/deactivation of MAP kinases p38 and INK Earlier studies conducted using cultured immortalized macrophages provided compelling evidence indicating that MKP-1 deactivates p38 and JNK, thereby limiting pro-inflammatory cytokine biosynthesis in innate immune cells exposed to microbial components. Recent studies employing MKP-1 knockout mice have confirmed the central function of MKP-1 in the feedback control of p38 and JNK activity as well as the crucial physiological function of MKP-1 as a negative regulator of the synthesis of pro-inflammatory cytokines in vivo. MKP-1 was shown to be a major feedback regulator of the innate immune response and to play a critical role in preventing septic shock and multi-organ dysfunction during pathogenic infection. In this review, we will update the studies on the biochemical properties and the regulation of MKP-1, and summarize our understanding on the physiological function of this key phosphatase in the innate immune response. (c) 2007 Elsevier Inc. All rights reserved.
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