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Updated: Feb 10, 2026

Hydrolysis of a Ni-Schiff-Base Complex Using Conditions Suitable for Retention of Acid-labile Protecting Groups
Published on: April 6, 2017
Vitamin D Switches BAF Complexes to Protect β Cells
Zong Wei1, Eiji Yoshihara1, Nanhai He1
1Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Vitamin D receptor (VDR) plays a crucial role in protecting pancreatic beta cells from inflammation and dysfunction in type 2 diabetes (T2D). Targeting VDR-chromatin interactions offers a new therapeutic strategy for T2D.
Area of Science:
- Endocrinology
- Molecular Biology
- Immunology
Background:
- Type 2 diabetes (T2D) is characterized by beta cell dysfunction, driven by inflammation and insulin resistance.
- Preventing beta cell exhaustion remains a significant therapeutic hurdle in managing T2D progression.
Purpose of the Study:
- To investigate the role of the vitamin D receptor (VDR) in regulating inflammation and beta cell survival.
- To identify VDR-associated protein complexes and their function in the context of T2D.
Main Methods:
- Investigated VDR interactions with bromodomain proteins (BRD7, BRD9) and chromatin remodeling complexes (PBAF, BAF).
- Analyzed VDR's genome-wide effects on chromatin accessibility and enhancer activity.
- Utilized pharmacological inhibition of BRD9 in murine models of T2D.
Main Results:
- VDR modulates inflammation and beta cell survival.
- VDR associates with PBAF chromatin remodeling complexes, mediated by acetylation and bromodomain proteins.
- Ligand-bound VDR promotes PBAF association, leading to anti-inflammatory effects.
- Inhibition of BRD9 enhances PBAF-VDR association, restoring beta cell function and improving hyperglycemia in diabetic mice.
Conclusions:
- Identified an uncharacterized VDR-dependent transcriptional pathway crucial for beta cell survival in T2D.
- The VDR:PBAF/BAF association represents a potential therapeutic target for T2D treatment.
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