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Diabetes Obes Metab. 2016 Sep;18 Suppl 1:123-7. doi: 10.1111/dom.12730.

Impact of Pdx1-associated chromatin modifiers on islet β-cells.

Author information

1
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee.
2
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee. roland.stein@vanderbilt.edu.

Abstract

Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β-cells. In type 2 diabetes (T2D), β-cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of pancreas development and islet β-cell formation, identity and function. TFs, like Pdx1, recruit coregulators to transduce activating and/or repressing signals to the general transcriptional machinery for controlling gene expression, including modifiers of DNA, histones and nucleosome architecture. These coregulators impart a secondary layer of control that can be exploited to modulate TF activity. In this review, we describe Pdx1-recruited coregulators that impact chromatin structure, consequently influencing normal β-cell function and likely Pdx1 activity in pathophysiological settings.

KEYWORDS:

Pdx1; coregulators; diabetes mellitus; islet-enriched transcription factors; type 2 diabetes; β-cell dysfunction

PMID:
27615141
PMCID:
PMC5918695
DOI:
10.1111/dom.12730
[Indexed for MEDLINE]
Free PMC Article

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