Jurczak Lab Publications
For a full list of publication, click here.
- G-protein coupled receptor 19 (GPR19) knockout mice display sex-dependent metabolic dysfunctionby Bellina A S Mushala on April 15, 2023 at 10:00 am
G-protein coupled receptors (GPCRs) mediate signal transduction from the cellular surface to intracellular metabolic pathways. While the function of many GPCRs has been delineated previously, a significant number require further characterization to elucidate their cellular function. G-protein coupled receptor 19 (GPR19) is a poorly characterized class A GPCR which has been implicated in the regulation of circadian rhythm, tumor metastasis, and mitochondrial homeostasis. In this report, we use a...
- Mitotic CDK1 and 4E-BP1 II: A single phosphomimetic mutation in 4E-BP1 induces glucose intolerance in miceby Simon Cao on March 10, 2023 at 11:00 am
CONCLUSIONS: 4E-BP1S82D is a single amino acid substitution that induces glucose intolerance in mice. These findings indicate that glucose metabolism may be regulated by CDK1 4E-BP1 phosphorylation independent from mTOR and point towards an unexpected role for cycling cells that transit mitosis in diabetic glucose control.
- Author Correction: Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitisby Josepmaria Argemi on February 10, 2023 at 11:00 am
No abstract
- Reduced hepatocyte mitophagy is an early feature of NAFLD pathogenesis and hastens the onset of steatosis, inflammation and fibrosisby Ramya Undamatla on January 30, 2023 at 11:00 am
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologies that includes steatosis, steatohepatitis (NASH) and fibrosis and is strongly associated with insulin resistance and type 2 diabetes. Changes in mitochondrial function are implicated in the pathogenesis of NAFLD, particularly in the transition from steatosis to NASH. Mitophagy is a mitochondrial quality control mechanism that allows for the selective removal of damaged mitochondria from the cell via the autophagy...
- Hepatocyte-derived GDF15 suppresses feeding and improves insulin sensitivity in obese miceby Bingxian Xie on December 5, 2022 at 11:00 am
Growth differentiation factor 15 (GDF15) is a stress-induced secreted protein whose circulating levels are increased in the context of obesity. Recombinant GDF15 reduces body weight and improves glycemia in obese models, which is largely attributed to the central action of GDF15 to suppress feeding and reduce body weight. Despite these advances in knowledge, the tissue-specific sites of GDF15 production during obesity are unknown, and the effects of modulating circulating GDF15 levels on insulin...