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Biochim Biophys Acta. 2007 Aug;1773(8):1341-8. Epub 2007 Jan 4.

The c-jun kinase/stress-activated pathway: regulation, function and role in human disease.

Author information

1
University of North Carolina at Chapel Hill, Department of Pharmacology, and Lineberger Comprehensive Cancer Center, 31-331 LCC Chapel Hill, NC 27599, USA. gary_johnson@med.unc.edu

Abstract

c-Jun N-terminal kinases (JNKs), also referred to as stress-activated kinases (SAPKs), were initially characterized by their activation in response to cell stress such as UV irradiation. JNK/SAPKs have since been characterized to be involved in proliferation, apoptosis, motility, metabolism and DNA repair. Dysregulated JNK signaling is now believed to contribute to many diseases involving neurodegeneration, chronic inflammation, birth defects, cancer and ischemia/reperfusion injury. In this review, we present our current understanding of JNK regulation and their involvement in homeostasis and dysregulation in human disease.

PMID:
17306896
PMCID:
PMC1995559
DOI:
10.1016/j.bbamcr.2006.12.009
[Indexed for MEDLINE]
Free PMC Article

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