c-Jun N-terminal phosphorylation antagonises recruitment of the Mbd3/NuRD repressor complex

Cristina Aguilera, Kentaro Nakagawa, Rocio Sancho, Atanu Chakraborty, Brian Hendrich and Axel Behrens ()
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Cristina Aguilera: Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln’s Inn Fields Laboratories, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK
Kentaro Nakagawa: Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln’s Inn Fields Laboratories, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK
Rocio Sancho: Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln’s Inn Fields Laboratories, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK
Atanu Chakraborty: Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln’s Inn Fields Laboratories, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK
Brian Hendrich: Wellcome Trust Centre for Stem Cell Research, Medical Research Council Centre for Stem Cell Biology and Regenerative Medicine, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK
Axel Behrens: Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln’s Inn Fields Laboratories, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK

Nature, 2011, vol. 469, issue 7329, 231-235

Abstract: JNK signalling mechanisms The JNK/c-Jun signalling pathway has been implicated in various diseases, including neurodegeneration, diabetes and cancer, and JNK inhibitors are seen as potential therapeutic agents. The mechanism by which the kinase JNK activates c-Jun has now been identified. N-terminal phosphorylation of c-Jun is shown to antagonize the interaction of c-Jun with Mbd3, a component of the repressor complex NuRD. The interaction between c-Jun and Mbd3 is shown to be important in regulating the proliferation of intestinal progenitor cells in mice.

Date: 2011
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DOI: 10.1038/nature09607

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