Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 40, Issue -, Pages 85-89Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST20110641
Keywords
cancer; c-Jun N-terminal kinase (JNK); mitogen-activated protein kinase (MAPK); mitogen-activated protein kinase kinase 4 (MKK4); mitogen-activated protein kinase kinase 7 (MKK7); neurodegeneration
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Funding
- Cancer Research UK [C18267/A11727]
- Association for International Cancer Research [10-0134]
- Alzheimer's Research UK [ART-PG2011-10]
- MRC [G0001285] Funding Source: UKRI
- Alzheimers Research UK [ART-PG2011-10] Funding Source: researchfish
- Medical Research Council [G0001285] Funding Source: researchfish
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INK (c-Jun N-terminal kinase) is a member of the MAPK (mitogen-activated protein kinase) family that regulates a range of biological processes implicated in tumorigenesis and neurodegenerative disorders. For example, genetic studies have demonstrated that the removal of specific Jnk genes can reduce neuronal death associated with cerebral ischaemia. As such, targeting JNK signalling constitutes an obvious opportunity for therapeutic intervention. However, MAPK inhibitors can display toxic effects. Consequently, dual-specificity MKKs (MAPK kinases) may represent more attractive targets. In particular, evidence that blocking JNK activation by removing MKK4 offers an effective therapy to treat pathological conditions has started to emerge. MKK4 was the first JNK activator identified. The remaining level of JNK activity in cells lacking MKK4 expression led to the discovery of a second activator of JNK, named MKK7. Distinct phenotypic abnormalities associated with the targeted deletion of Mkk4 and Mkk7 in mice have revealed that MKK4 and MKK7 have non-redundant function in vivo. Further insights into the specific functions of the JNK activators in cancer cells and in neurons will be of critical importance to validate MKK4 and MKK7 as promising drug targets.
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