Metabolic stress activates an ERK/hnRNPK/DDX3X pathway in pancreatic β cells.

ABSTRACT:

Objective

Pancreatic β cell failure plays a central role in the development of type 2 diabetes (T2D). While the transcription factors shaping the β cell gene expression program have received much attention, the post-transcriptional controls that are activated in β cells during stress are largely unknown. We recently identified JUND as a pro-oxidant transcription factor that is post-transcriptionally upregulated in β cells during metabolic stress. Here we seek to uncover the mechanisms underlying this maladaptive response to metabolic stress.

Methods

RNA-protein and protein-protein interactions were measured using RNA immunoprecipitation and co-immunoprecipitation, respectively, in Min6 cells and mouse islets. Phos-tag analyses were used to assess hnRNPK phosphorylation in pr

SUBMITTER: Good AL 

PROVIDER: S-EPMC6667393 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature