Ligand-dependent nuclear receptor corepressor LCoR functions by histone deacetylase-dependent and -independent mechanisms - PubMed (original) (raw)

doi: 10.1016/s1097-2765(03)00014-5.

Yolande Bastien, Timothy Wai, Karen Nygard, Roberto Lin, Olivier Cormier, Han S Lee, Frankie Eng, Nicholas R Bertos, Nadine Pelletier, Sylvie Mader, Victor K M Han, Xiang-Jiao Yang, John H White

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• PMID: 12535528
• DOI: 10.1016/s1097-2765(03)00014-5

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Ligand-dependent nuclear receptor corepressor LCoR functions by histone deacetylase-dependent and -independent mechanisms

Isabelle Fernandes et al. Mol Cell. 2003 Jan.

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Abstract

LCoR (ligand-dependent corepressor) is a transcriptional corepressor widely expressed in fetal and adult tissues that is recruited to agonist-bound nuclear receptors through a single LXXLL motif. LCoR binding to estrogen receptor alpha depends in part on residues in the coactivator binding pocket distinct from those bound by TIF-2. Repression by LCoR is abolished by histone deacetylase inhibitor trichostatin A in a receptor-dependent fashion, indicating HDAC-dependent and -independent modes of action. LCoR binds directly to specific HDACs in vitro and in vivo. Moreover, LCoR functions by recruiting C-terminal binding protein corepressors through two consensus binding motifs and colocalizes with CtBPs in the nucleus. LCoR represents a class of corepressor that attenuates agonist-activated nuclear receptor signaling by multiple mechanisms.

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