Coronin 2A mediates actin-dependent de-repression of inflammatory response genes

Wendy Huang, Serena Ghisletti, Kaoru Saijo, Meghal Gandhi, Myriam Aouadi, Greg J. Tesz, Dawn X. Zhang, Joyee Yao, Michael P. Czech, Bruce L. Goode, Michael G. Rosenfeld and Christopher K. Glass ()
Additional contact information
Wendy Huang: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Serena Ghisletti: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Kaoru Saijo: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Meghal Gandhi: Rosenstiel Basic Medical Science Research Center, Brandeis University
Myriam Aouadi: Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, Massachusetts 01605, USA
Greg J. Tesz: Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, Massachusetts 01605, USA
Dawn X. Zhang: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Joyee Yao: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Michael P. Czech: Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, Massachusetts 01605, USA
Bruce L. Goode: Rosenstiel Basic Medical Science Research Center, Brandeis University
Michael G. Rosenfeld: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA
Christopher K. Glass: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA

Nature, 2011, vol. 470, issue 7334, 414-418

Abstract: Control of inflammatory responses Activation of inflammatory gene expression by toll-like receptor (TLR) signalling pathways involves the removal of gene repression complexes such as NCoR. Coronin 2A, a component of the NCoR complex, is now shown to mediate TLR-induced NCoR turnover and de-repression of inflammatory genes by a mechanism involving interaction with oligomeric nuclear actin. This work points to a role for an actin-dependent mechanism in the de-repression of TLR target genes that is regulated by phosphorylation and nuclear receptor signalling pathways to differentially control inflammatory responses.

Date: 2011
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DOI: 10.1038/nature09703

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