A5026419033- PI3K/AKT/mTOR signaling in cancer
- Ubiquitin and proteasome pathways
- Polyamine Metabolism and Applications
- Cytokine Signaling Pathways and Interactions
- Endoplasmic Reticulum Stress and Disease
- Metabolism, Diabetes, and Cancer
- Genetics, Bioinformatics, and Biomedical Research
- Liver physiology and pathology
- Pancreatic function and diabetes
- Toxin Mechanisms and Immunotoxins
- Protein Kinase Regulation and GTPase Signaling
- CRISPR and Genetic Engineering
- Magnetic and Electromagnetic Effects
- Neurobiology and Insect Physiology Research
- Genomics, phytochemicals, and oxidative stress
- Protein Structure and Dynamics
- Regulation of Appetite and Obesity
- Cancer Mechanisms and Therapy
- Glycosylation and Glycoproteins Research
- Hedgehog Signaling Pathway Studies
- Sirtuins and Resveratrol in Medicine
- Diabetes Treatment and Management
- Cell Adhesion Molecules Research
University of Michigan
2019-2024
Abstract Exercise is among the most effective interventions for age-associated mobility decline and metabolic dysregulation. Although long-term endurance exercise promotes insulin sensitivity expands respiratory capacity, genetic components pathways mediating benefits of have remained elusive. Here, we show that Sestrins, a family evolutionarily conserved exercise-inducible proteins, are critical mediators benefits. In both fly mouse models, ablation Sestrins prevents organisms from...
Sestrins represent a family of stress-inducible proteins that prevent the progression many age- and obesity-associated disorders. Endogenous maintain insulin-dependent AKT Ser/Thr kinase (AKT) activation during high-fat diet–induced obesity, overexpressed activate in various cell types, including liver skeletal muscle cells. Although Sestrin-mediated improves metabolic parameters, mechanistic details underlying such improvement remain elusive. Here, we investigated how Sestrin2, Sestrin...
mTORC1 is a protein kinase important for metabolism and regulated by growth factor nutrient signaling pathways, mediated the Rheb Rag GTPases, respectively. Here we provide first animal model in which both pathways were upregulated through concurrent mutations their GTPase-activating proteins, Tsc1 Depdc5. Unlike former models that induced limited upregulation, hepatic deletion of Depdc5 (DKO) produced strong, synergistic activation pathway provoked pronounced widespread hepatocyte damage,...