Journal
CYTOKINE
Volume 48, Issue 3, Pages 161-169Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2009.08.002
Keywords
Kinase; Phosphatase; Signaling; Receptor; Immunity
Funding
- US National Institutes of Health [R01 NS064599]
- Cancer Center Support [CA021765]
- National Multiple Sclerosis [RG4180-A-1]
- Hartwell Foundation Individual Biomedical Research Award
- Cancer Research Institute Investigator Award
- American Lebanese Syrian Associated Charities
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Stress-activated MAP kinases (MAPKs), comprised of JNK and p38, play prominent roles in the innate and adaptive immune systems. Activation of MAPKs is mediated by a three-tiered kinase module comprised of MAPK kinase kinases (MAP3Ks), MAPK kinases (MAP2Ks) and MAPKs through sequential protein phosphorylation. Activated MAPKs, in turn, phosphorylate transcription factors and other targets to regulate gene transcription and immune responses. Recent studies have provided new insight into the upstream and downstream components of the MAPK pathway that facilitate the activation and propagation of MAPK signaling in immune responses. Moreover, MAPK activity is negatively regulated by MAPK phosphatases (MKPs), a group of dual-specificity phosphatases that dephosphorylate and inactivate the MAPKs. Here we discuss the recent advances in our understanding of these regulatory processes in MAPK signaling with a focus on their impacts on immune function. (C) 2009 Elsevier Ltd. All rights reserved
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