ReviewDiabetologia2015
Roles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscle.
Review in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
95 citing papers in PubMed, 143 citations in OpenAlex.
- Phosphoproteomics Uncovers Exercise Intensity-Specific Skeletal Muscle Signaling Networks Underlying High-Intensity Interval Training in Healthy Male Participants.Sports medicine (Auckland, N.Z.) · 2025Trial
- The Impact of Body Resistance Training Exercise on Biomedical Profile at High Altitude: A Randomized Controlled Trial.BioMed research international · 2021Trial
- Preexercise breakfast ingestion versus extended overnight fasting increases postprandial glucose flux after exercise in healthy men.American journal of physiology. Endocrinology and metabolism · 2018Trial
- Electrical Pulse Stimulation Partially Restores Insulin Signaling in Palmitate-Induced Insulin-Resistant Skeletal Muscle Cells via Mitochondrial Remodeling and Contractile Activity-Dependent Secretome.Journal of cellular physiology · 2026Article
- Quantitative interactome mapping of skeletal muscle insulin resistance.Molecular systems biology · 2026Article
- WNK1 Phosphorylation Sites in TBC1D1 and TBC1D4 Modulate Cell-Surface Abundance of GLUT1.Cells · 2026Article
- TBC1D4-Related Monogenic Diabetes: Molecular Mechanisms, Clinical Recognition, and Therapeutic Implications.Journal of diabetes · 2026Review
- Seeking the Mechanism for Reversal of Enhanced Insulin Sensitivity After Acute Exercise.Exercise and sport sciences reviews · 2026Review
- Long-term isolation and archaic introgression shape functional genetic variation in Near Oceania.Science (New York, N.Y.) · 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
- Canonical and Alternative Pathways (Insulin and Exercise) of GLUT4 Synthesis, Signaling, Intracellular Clustering, and Recruitment to the Plasma Membrane.International journal of molecular sciences · 2026Review
- Pan-3D Genome Analysis Reveals the Roles of Structural Variation in Chicken Chromatin Architectures, Domestication and Production Traits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Japanese encephalitis virus orchestrates GLUT4-mediated glucose metabolism to potentiate viral replication via insulin receptor signaling.PLoS pathogens · 2026Article
- Interpretable integration of unpaired multi-omics for Alzheimer's diagnosis via cross-modal transformer reconstruction.PLoS computational biology · 2026Article
- Inhibition of p38 MAPK after repetitive mTBI ameliorates immune signaling and functional deficits.Acta neuropathologica communications · 2026Article
- The metabolic role of corticotropin-releasing hormone receptor 2 and its UCN peptides: emerging therapeutic potential.Skeletal muscle · 2025Review
- Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice.Journal of sport and health science · 2025Article
- Neurogranin-MYH9 interaction regulates cytoskeletal remodeling in cerebral vasculature.Fluids and barriers of the CNS · 2025Article
- Implications and Applications of Stretch-Mediated Hypertrophy in Therapy, Rehabilitation and Athletic Training-An Outlook to Future Potential Applications.Sports medicine (Auckland, N.Z.) · 2025Article
- Unraveling Skeletal Muscle Insulin Resistance: Molecular Mechanisms and the Restorative Role of Exercise.Circulation research · 2025Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
This review focuses on two paralogue Rab GTPase activating proteins known as TBC1D1 Tre-2/BUB2/cdc 1 domain family (TBC1D) 1 and TBC1D4 (also called Akt Substrate of 160 kDa, AS160) and their roles in controlling skeletal muscle glucose transport in response to the independent and combined effects of insulin and exercise. Convincing evidence implicates Akt2-dependent TBC1D4 phosphorylation on T642 as a key part of the mechanism for insulin-stimulated glucose uptake by skeletal muscle. TBC1D1 phosphorylation on several insulin-responsive sites (including T596, a site corresponding to T642 in TBC1D4) does not appear to be essential for in vivo insulin-stimulated glucose uptake by skeletal muscle. In vivo exercise or ex vivo contraction of muscle result in greater TBC1D1 phosphorylation on S237 that is likely to be secondary to increased AMP-activated protein kinase activity and potentially important for contraction-stimulated glucose uptake. Several studies that evaluated both normal and insulin-resistant skeletal muscle stimulated with a physiological insulin concentration after a single exercise session found that greater post-exercise insulin-stimulated glucose uptake was accompanied by greater TBC1D4 phosphorylation on several sites. In contrast, enhanced post-exercise insulin sensitivity was not accompanied by greater insulin-stimulated TBC1D1 phosphorylation. The mechanism for greater TBC1D4 phosphorylation in insulin-stimulated muscles after acute exercise is uncertain, and a causal link between enhanced TBC1D4 phosphorylation and increased post-exercise insulin sensitivity has yet to be established. In summary, TBC1D1 and TBC1D4 have important, but distinct roles in regulating muscle glucose transport in response to insulin and exercise.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.