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

Biochim Biophys Acta. 2007 Aug;1773(8):1341-8. doi: 10.1016/j.bbamcr.2006.12.009. Epub 2007 Jan 4.


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.

Publication types

  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Disease / etiology
  • Female
  • Hearing Loss / enzymology
  • Humans
  • Inflammation / enzymology
  • JNK Mitogen-Activated Protein Kinases / chemistry
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism*
  • Liver / blood supply
  • Liver / injuries
  • MAP Kinase Signaling System
  • Models, Biological
  • Molecular Sequence Data
  • Neoplasms / enzymology
  • Neural Tube Defects / enzymology
  • Neurodegenerative Diseases / enzymology
  • Pregnancy
  • Reperfusion Injury / enzymology
  • Reperfusion Injury / etiology
  • Sequence Homology, Amino Acid
  • Signal Transduction


  • JNK Mitogen-Activated Protein Kinases