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Impact of Pdx1‐associated chromatin modifiers on islet β‐cells
Author(s) -
Spaeth J. M.,
Walker E. M.,
Stein R.
Publication year - 2016
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.12730
Subject(s) - pdx1 , chromatin , histone , transcription factor , regulator , islet , microbiology and biotechnology , biology , pancreas , nucleosome , endocrinology , insulin , gene , genetics
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.