Roland W. Stein

This study shows that MAFB is essential for maintaining adult human α-cell identity and function, linking its downregulation to impaired glucagon secretion and mitochondrial dysfunction in diabetes.

This study shows MYT1 and ST18 regulate human beta-cell survival and insulin secretion under normal and stress conditions, with their genes enriched for T2D-risk loci.

This study shows that genetic background affects disease penetrance in MafAS64F/+ male mice, with C57 background preventing dysglycemia while mixed background leads to diabetes and beta-cell senescence.

This study shows Atf4 protects beta-cell function under high glucose but worsens beta-cell failure when combined with free fatty acids.

The paper identifies structural features in MAFA and MAFB transcription factors that influence their DNA-binding and Insulin enhancer activity through structural and functional analysis.

This paper identifies a MAFA S64F variant causing sex-dependent β cell dysfunction and diabetes by accelerating aging and senescence in males.

The paper identifies combinatorial transcription factor expression in human islet cells and shows it correlates with functional maturity and electrophysiological activity.

This study shows that Myt transcription factors prevent over-activation of stress-response genes in pancreatic β cells, maintaining their function and survival.