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Acetylation of lysine 109 modulates pregnane X receptor DNA binding and transcriptional activity
Journal article   Open access   Peer reviewed

Acetylation of lysine 109 modulates pregnane X receptor DNA binding and transcriptional activity

Danielle Pasquel, Aneta Doricakova, Hao Li, Sandhya Kortagere, Matthew D Krasowski, Arunima Biswas, William G Walton, Matthew R Redinbo, Zdenek Dvorak and Sridhar Mani
Biochimica et biophysica acta. Gene regulatory mechanisms, Vol.1859(9), pp.1155-1169
09/2016
DOI: 10.1016/j.bbagrm.2016.01.006
PMCID: PMC4975685
PMID: 26855179
url
http://doi.org/10.1016/j.bbagrm.2016.01.006View
Open Access

Abstract

Pregnane X receptor (PXR) is a major transcriptional regulator of xenobiotic metabolism and transport pathways in the liver and intestines, which are critical for protecting organisms against potentially harmful xenobiotic and endobiotic compounds. Inadvertent activation of drug metabolism pathways through PXR is known to contribute to drug resistance, adverse drug–drug interactions, and drug toxicity in humans. In both humans and rodents, PXR has been implicated in non-alcoholic fatty liver disease, diabetes, obesity, inflammatory bowel disease, and cancer. Because of PXR's important functions, it has been a therapeutic target of interest for a long time. More recent mechanistic studies have shown that PXR is modulated by multiple PTMs. Herein we provide the first investigation of the role of acetylation in modulating PXR activity. Through LC–MS/MS analysis, we identified lysine 109 (K109) in the hinge as PXR's major acetylation site. Using various biochemical and cell-based assays, we show that PXR's acetylation status and transcriptional activity are modulated by E1A binding protein (p300) and sirtuin 1 (SIRT1). Based on analysis of acetylation site mutants, we found that acetylation at K109 represses PXR transcriptional activity. The mechanism involves loss of RXRα dimerization and reduced binding to cognate DNA response elements. This mechanism may represent a promising therapeutic target using modulators of PXR acetylation levels. This article is part of a Special Issue entitled: Xenobiotic nuclear receptors: New Tricks for An Old Dog, edited by Dr. Wen Xie. [Display omitted] •p300 acetylates pregnane X receptor (PXR) at lysine (K) 109.•Acetylation at K109 negatively regulates DNA binding and transcriptional activity.•Acetylation acts to fine-tune PXR activity. [Display omitted]
Drug Metabolism Nuclear receptor Pregnane X receptor (PXR) Acetylation E1A binding protein p300 (p300) Post-translational modification (PTM) Transcription regulation

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