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

Spaeth JM, Walker EM, Stein R
Diabetes Obes Metab. 2016 18 Suppl 1: 123-7

PMID: 27615141 · PMCID: PMC5918695 · DOI:10.1111/dom.12730

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.

© 2016 John Wiley & Sons Ltd.

MeSH Terms (12)

Animals Chromatin Assembly and Disassembly Diabetes Mellitus, Type 2 DNA Methylation Gene Expression Regulation Histone Code Homeodomain Proteins Humans Insulin-Secreting Cells Mice Nucleosomes Trans-Activators

Connections (1)

This publication is referenced by other Labnodes entities:

Links