Histone NRlator Project: Defining the histone coregulator interactome

Rakesh Kumar Department of Biochemistry & Molecular Biology

Sujit Nair Department of Biochemistry & Molecular Biology

Norman Lee Department of Pharmacology & Physiology

Weiqun Peng Department of Physic

The Nuclear Receptor Signaling Atlas (NURSA) Consortium (www.NURSA.org) is a NIH consortium supported by the National Institute of Diabetes and Digestive & Kidney diseases (NIDDK), National Heart Lung and Blood Institute (NHLBI) and National Institute of Environmental Health Sciences (NIEHS). The mission of the NURSA consortium is to develop large datasets and new knowledge and further the cause of education in the areas of the nuclear receptors and coregulators.

Early in 2010, Rakesh Kumar and his team have been invited to join the membership of the NURSA as an Associate member. The current members of the NURSA include Bert O’Malley (NAS member, US National Medal of Science holder at the Baylor College of Medicine), Ron Evans (NAS member at the Salk Institute), David Mangelsdorf (NAS member at the University of Texas Southwestern Medical Center), Chris Glass (University of California at San Diego), and Mitch Lazer (University of Pennsylvania). The newly added Histone-NRlator project from the George Washington University is part of the Proteomic Strand of the consortium; other two strands include Genomic, and Bioinformatics.

The goal of the Histone-NRlator project is to provide a comprehensive data set of histone-NR coregulator interactomes. A better understanding of the ability of NR coregulators to recognize key histone modifications in the context of cellular signaling and specific post-translational modifications will produce novel insights into how these proteins regulate biological processes, such as genomic surveillance, imprinting, transcriptional memory, and DNA-damage response. The Histone-NRlator project is designed to catalogue the genomic localization and binding of prototypic NR coregulators to modified or unmodified histones in response to genotoxic stress.

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