Transcriptional activation of the Myc gene by glucose in β-cells requires a ChREBP-dependent 3-D chromatin interaction between the Myc and Pvt1 genes.

ABSTRACT:

Objective

All forms of diabetes result from insufficient functional β-cell mass. Thus, achieving the therapeutic goal of expanding β-cell mass requires a better mechanistic understanding of how β-cells proliferate. Glucose is a natural β-cell mitogen that mediates its effects in part through the glucose-responsive transcription factor, carbohydrate response element binding protein (ChREBP) and the anabolic transcription factor, MYC. However, mechanistic details by which glucose activates Myc at the transcriptional level are poorly understood.

Methods

Here, siRNA was used to test the role of ChREBP in the glucose response of MYC, ChIP and ChIPseq to identify potential regulatory binding sites, chromatin conformation capture to identify DNA/DNA interactions, and an adenovirus

SUBMITTER: Katz LS 

PROVIDER: S-EPMC10714240 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature