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Title: Impact of Pdx1-associated chromatin modifiers on islet β-cells. Author: Spaeth JM, Walker EM, Stein R. Journal: Diabetes Obes Metab; 2016 Sep; 18 Suppl 1(Suppl 1):123-7. PubMed ID: 27615141. 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.[Abstract] [Full Text] [Related] [New Search]