The c-jun kinase/stress-activated pathway: regulation, function and role in human disease.
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.
Johnson
Gary L
GL
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
Nakamura
Kazuhiro
K
D000595:Amino Acid Sequence; D000818:Animals; D004194:Disease / Q000209:etiology; D005260:Female; D034381:Hearing Loss / Q000201:enzymology; D006801:Humans; D007249:Inflammation / Q000201:enzymology; D048031:JNK Mitogen-Activated Protein Kinases / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000098:blood supply / Q000293:injuries; D020935:MAP Kinase Signaling System; D008954:Models, Biological; D008969:Molecular Sequence Data; D009369:Neoplasms / Q000201:enzymology; D009436:Neural Tube Defects / Q000201:enzymology; D019636:Neurodegenerative Diseases / Q000201:enzymology; D011247:Pregnancy; D015427:Reperfusion Injury / Q000201:enzymology / Q000209:etiology; D017386:Sequence Homology, Amino Acid; D015398:Signal Transduction
D048031:JNK Mitogen-Activated Protein Kinases