Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

JNK Subfamily

Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_3184-2

Synonyms

Definition

JNK is an intracellular protein kinase that transmits rapidly and efficiently various different types of signals originating from outside of a cell in the process called signal transduction. Like other protein kinases, JNK is an enzyme that transmits its signals via phosphorylating its specific substrate proteins. The most studied JNK substrate is c-Jun, a component of the dimeric transcription factor AP-1, which gives rise to its name: c-Jun N-terminal kinase. Another name for JNK is a stress-activated protein kinase (SAPK). The p38 MAPKs are also called SAPKs, and thus, the term SAPK actually refers to both JNK and p38 subfamilies.

Characteristics

JNK subfamily consists of three isoforms: JNK1, JNK2, and JNK3. They are encoded by three separate genes: MAPK8, MAPK9, and MAPK10. Alternative splicing of these genes can produce at least ten different...

Keywords

Splice Variant Skin Carcinogenesis Intracellular Protein Kinase Specific Substrate Protein JNK2 Knockout 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Bogoyevitch MA, Kobe B (2006) Uses of JNK: the many and varied substrates of the c-Jun N-terminal kinases. Microbiol Mol Biol Rev 70:1061–1095CrossRefPubMedPubMedCentralGoogle Scholar
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  3. Engelberg D (2004) Stress-activated protein kinases-tumor suppressors or tumor initiators? Semin Cancer Biol 14:271–282CrossRefPubMedGoogle Scholar
  4. Johnson GL, Nakamura K (2007) The c-jun kinase/stress-activated pathway: regulation, function and role in human disease. Biochem Biophys Acta 1773:1341–1348CrossRefPubMedPubMedCentralGoogle Scholar
  5. Karin M, Gallagher E (2005) From JNK to pay dirt: jun kinases, their biochemistry, physiology and clinical importance. IUBMB Life 57:283–295CrossRefPubMedGoogle Scholar
  6. Morrison DK, Davis RJ (2003) Regulation of MAP kinase signaling modules by scaffold proteins in mammals. Annu Rev Cell Dev Biol 19:91–118CrossRefPubMedGoogle Scholar

See Also

  1. (2012) AKT. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 115. doi: 10.1007/978-3-642-16483-5_163Google Scholar
  2. (2012) ATF2. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 299. doi: 10.1007/978-3-642-16483-5_429Google Scholar
  3. (2012) Dominant negative. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1150. doi: 10.1007/978-3-642-16483-5_1705Google Scholar
  4. (2012) Isoform. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, pp 1920–1921. doi: 10.1007/978-3-642-16483-5_3158Google Scholar
  5. (2012) JNK cascade. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1927. doi: 10.1007/978-3-642-16483-5_3183Google Scholar
  6. (2012) Knock-out mouse. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 1957. doi: 10.1007/978-3-642-16483-5_3239Google Scholar
  7. (2012) Max. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 2188. doi: 10.1007/978-3-642-16483-5_3565Google Scholar
  8. (2012) P53. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 2747. doi: 10.1007/978-3-642-16483-5_4331Google Scholar
  9. (2012) Programmed cell death. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 2994. doi: 10.1007/978-3-642-16483-5_4760Google Scholar
  10. (2012) Splicing. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3487. doi: 10.1007/978-3-642-16483-5_5456Google Scholar
  11. (2012) TPA. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3740. doi: 10.1007/978-3-642-16483-5_5878Google Scholar
  12. (2012) Tumor SUPPRESSOR. In: Schwab M (ed) Encyclopedia of cancer, 3rd edn. Springer, Berlin/Heidelberg, p 3803. doi: 10.1007/978-3-642-16483-5_6056Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Unit of Cell Death and MetabolismDanish Cancer Society Research CenterCopenhagenDenmark