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Nat Rev Drug Discov. 2003 Jul;2(7):554-65.

Targeting JNK for therapeutic benefit: from junk to gold?

Author information

1
Roche Pharmaceuticals, 3411 Hillview Avenue, Palo Alto, CA 94306, USA. anthony.manning@roche.com

Abstract

The c-Jun NH(2)-terminal kinases (JNKs) phosphorylate and activate members of the activator protein-1 (AP-1) transcription factor family and other cellular factors implicated in regulating altered gene expression, cellular survival and proliferation in response to cytokines and growth factors, noxious stimuli and oncogenic transformation. Because these events are commonly associated with the pathogenesis of a number of human diseases, the potential of JNK inhibitors as therapeutics has attracted considerable interest. Here we discuss the evidence supporting the application of JNK inhibitors in inflammatory, vascular, neurodegenerative, metabolic and oncological diseases in humans, and describe the present status of drug discovery targeting JNK.

PMID:
12815381
DOI:
10.1038/nrd1132
[Indexed for MEDLINE]

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