ArticleCell death and differentiation2021
AMPK-mediated phosphorylation enhances the auto-inhibition of TBC1D17 to promote Rab5-dependent glucose uptake.
Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Complementary intra- and extracellular AGR2 activities support epithelial ovarian cancer cell aggressiveness.Oncogene · 2026Article
- Quantitative interactome mapping of skeletal muscle insulin resistance.Molecular systems biology · 2026Article
- Structural and functional insights into TBC1D17 highlight the importance of the previously uncharacterized Rab-binding domain.Protein science : a publication of the Protein Society · 2026Article
- Rab5 nucleotide binding promotes oxidative metabolism to fuel hepatocellular carcinoma cell proliferation.The Journal of biological chemistry · 2026Article
- Lipid turnover and GEF recruitment collectively determine Rab5 recruitment and activation during the first step of early endosome formation.Nature communications · 2026Article
- Receptor-Interacting Protein Kinase 1 (RIPK1): A Potential Therapeutic Target in Ischemic Stroke.Molecular neurobiology · 2026Review
- Exercise benefits in metabolism on cardiovascular disease.Frontiers in cardiovascular medicine · 2026Review
- The role of AMPK signaling pathway in the pathogenesis of type 2 diabetes mellitus with its complications and related metabolic disorders.Metabolism open · 2025Review
- Article
- Potential Drug Targets for Migraine Identified Through Mendelian Randomization Analysis of the Human Plasma Proteome.Molecular neurobiology · 2025Article
- TBC1D22B Regulates ER-to-Golgi Trafficking via RAB1B Inactivation and Promotes Oncogenic Programs in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanism and cellular actions of the potent AMPK inhibitor BAY-3827.Science advances · 2025Article
- Phosphorylation of Golgin Imh1 by AMPK/Snf1 compromises Golgi compartmentalization by releasing Arl1-Imh1 axis.Molecular biology of the cell · 2025Article
- Deep and Quantitative Proteomic Profiling of Low Volume Mouse Serum Across the Lifespan.Research square · 2025Article
- KPNA3 regulates histone locus body formation by modulating condensation and nuclear import of NPAT.The Journal of cell biology · 2025Article
- Marine N-3 Fatty Acids Mitigate Hyperglycemia in Prediabetes by Improving Muscular Glucose Transporter 4 Translocation and Glucose Homeostasis.Research (Washington, D.C.) · 2025Article
- Article
- Targeting osteoblastic 11β-HSD1 to combat high-fat diet-induced bone loss and obesity.Nature communications · 2024Article
- Genomic Amplification of TBC1D31 Promotes Hepatocellular Carcinoma Through Reducing the Rab22A-Mediated Endolysosomal Trafficking and Degradation of EGFR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
Dysregulation of glucose homeostasis contributes to insulin resistance and type 2 diabetes. Whilst exercise stimulated activation of AMP-activated protein kinase (AMPK), an important energy sensor, has been highlighted for its potential to promote insulin-stimulated glucose uptake, the underlying mechanisms for this remain largely unknown. Here we found that AMPK positively regulates the activation of Rab5, a small GTPase which is involved in regulating Glut4 translocation, in both myoblasts and skeletal muscles. We further verified that TBC1D17, identified as a potential interacting partner of Rab5 in our recent study, is a novel GTPase activating protein (GAP) of Rab5. TBC1D17-Rab5 axis regulates transport of Glut1, Glut4, and transferrin receptor. TBC1D17 interacts with Rab5 or AMPK via its TBC domain or N-terminal 1-306 region (N-Ter), respectively. Moreover, AMPK phosphorylates the Ser 168 residue of TBC1D17 which matches the predicted AMPK consensus motif. N-Ter of TBC1D17 acts as an inhibitory region by directly interacting with the TBC domain. Ser168 phosphorylation promotes intra-molecular interaction and therefore enhances the auto-inhibition of TBC1D17. Our findings reveal that TBC1D17 acts as a molecular bridge that links AMPK and Rab5 and delineate a previously unappreciated mechanism by which the activation of TBC/RabGAP is regulated.
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