N-terminal BET bromodomain inhibitors disrupt a BRD4-p65 interaction and reduce inducible nitric oxide synthase transcription in pancreatic β-cells

N-terminal BET bromodomain inhibitors disrupt a BRD4-p65 interaction and reduce inducible nitric oxide synthase transcription in pancreatic β-cells

Chronic inflammation of pancreatic islets is a key driver of β-cell damage that can lead to autoreactivity and the eventual onset of autoimmune diabetes (T1D). In the islet, elevated levels of proinflammatory cytokines induce the transcription of the inducible nitric oxide synthase (iNOS) gene, NOS2...

Full description

Bibliographic Details
Main Authors: Joshua A. Nord, Sarah L. Wynia-Smith, Alyssa L. Gehant, Rachel A. Jones Lipinski, Aaron Naatz, Inmaculada Rioja, Rab K. Prinjha, John A. Corbett, Brian C. Smith
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-09-01
Series:Frontiers in Endocrinology
Subjects:
BET bromodomain
BRD4
diabetes
small molecule inhibitor
iNOS
nitric oxide
Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2022.923925/full

Internet

https://www.frontiersin.org/articles/10.3389/fendo.2022.923925/full

Similar Items