Inflammatory mediators increase SUMOylation of retinoid X receptor α in a c-Jun N-terminal kinase-dependent manner in human hepatocellular carcinoma cells.

ABSTRACT: Retinoid X receptor α [RXRα; nuclear receptor (NR)2B1] is a crucial regulator in the expression of a broad array of hepatic genes under both normal and pathologic conditions. During inflammation, RXRα undergoes rapid post-translational modifications, including c-Jun N-terminal kinase (JNK)-mediated phosphorylation, which correlates with a reduction in RXRα function. A small ubiquitin-like modifier (SUMO) acceptor site was recently described in human RXRα, yet the contributors, regulators, and consequences of SUMO-RXRα are not well understood. Inflammation and other stressors alter nuclear receptor function in liver and induce SUMOylation of several NRs as part of proinflammatory gene regulation, but linkages between these two pathways in liver, or for RXRα directly, remain unexplored. We s

SUBMITTER: Schneider Aguirre R 

PROVIDER: S-EPMC3716323 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature