The Contribution of Transcriptional Coregulators in the Maintenance of [beta]-cell Function and Identity

Islet [beta]-cell dysfunction that leads to impaired insulin secretion is a principal source of pathology of diabetes. In type 2 diabetes, this breakdown in [beta]-cell health is associated with compromised islet-enriched transcription factor (TF) activity that disrupts gene expression programs esse...

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Bibliographic Details
Published inEndocrinology (Philadelphia) Vol. 162; no. 2; p. 1
Main Authors Davidson, Rebecca K, Kanojia, Sukrati, Spaeth, Jason M
Format Journal Article
LanguageEnglish
Published Oxford University Press 01.02.2021
Subjects
B cells
DNA binding proteins
Genetic aspects
Genetic transcription
Histones
Type 2 diabetes
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Summary:Islet [beta]-cell dysfunction that leads to impaired insulin secretion is a principal source of pathology of diabetes. In type 2 diabetes, this breakdown in [beta]-cell health is associated with compromised islet-enriched transcription factor (TF) activity that disrupts gene expression programs essential for cell function and identity. TF activity is modulated by recruited coregulators that govern activation and/or repression of target gene expression, thereby providing a supporting layer of control. To date, more than 350 coregulators have been discovered that coordinate nucleosome rearrangements, modify histones, and physically bridge general transcriptional machinery to recruited TFs; however, relatively few have been attributed to [beta]-cell function. Here, we will describe recent findings on those coregulators with direct roles in maintaining islet [beta]-cell health and identity and discuss how disruption of coregulator activity is associated with diabetes pathogenesis. Key Words: islet, [beta]-cell identity, [beta]-cell function, transcription, coregulator
ISSN:0013-7227
1945-7170
DOI:10.1210/endocr/bqaa213