ArticleThe Journal of cell biology2016
SEC16A is a RAB10 effector required for insulin-stimulated GLUT4 trafficking in adipocytes.
Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
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- Cell-specific DNA methylation in human alpha and beta cells regulates gene expression in type 2 diabetes.Nature metabolism · 2026Article
- Construction of pathogenic Sec16a mutation mouse model using CRISPR/Cas9.Animal models and experimental medicine · 2026Article
- GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance.International journal of molecular sciences · 2025Review
- Cell-intrinsic insulin signaling defects in human iPS cell-derived hepatocytes in type 2 diabetes.The Journal of clinical investigation · 2025Article
- SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER-to-Golgi Transport and Inducing ER Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Genetic variation in NOTCH1 is associated with overweight and obesity in Brazilian elderly.Scientific reports · 2024Article
- Proteomics Analysis of Pregnancy in Ewes under Heat Stress Conditions and Melatonin Administration.Animals : an open access journal from MDPI · 2024Article
- Regulated dynamic subcellular GLUT4 localization revealed by proximal proteome mapping in human muscle cells.Journal of cell science · 2023Article
- Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.eLife · 2023Article
- Geranylgeranyl pyrophosphate depletion by statins compromises skeletal muscle insulin sensitivity.Journal of cachexia, sarcopenia and muscle · 2022Article
- GLUT4 On the move.The Biochemical journal · 2022Article
- Ubiquitin-like processing of TUG proteins as a mechanism to regulate glucose uptake and energy metabolism in fat and muscle.Frontiers in endocrinology · 2022Review
- Beta-Sitosterol Facilitates GLUT4 Vesicle Fusion on the Plasma Membrane via the Activation of Rab/IRAP/Munc 18 Signaling Pathways in Diabetic Gastrocnemius Muscle of Adult Male Rats.Bioinorganic chemistry and applications · 2022Article
- Rab GTPases: The principal players in crafting the regulatory landscape of endosomal trafficking.Computational and structural biotechnology journal · 2022Review
- Endosomal traffic and glutamate synapse activity are increased in VPS35 D620N mutant knock-in mouse neurons, and resistant to LRRK2 kinase inhibition.Molecular brain · 2021Article
- RIPK3 modulates growth factor receptor expression in endothelial cells to support angiogenesis.Angiogenesis · 2021Article
- Targeting Small GTPases and Their Prenylation in Diabetes Mellitus.Journal of medicinal chemistry · 2021Review
- Lithium enhances exercise-induced glycogen breakdown and insulin-induced AKT activation to facilitate glucose uptake in rodent skeletal muscle.Pflugers Archiv : European journal of physiology · 2021Article
- Rab family of small GTPases: an updated view on their regulation and functions.The FEBS journal · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
RAB10 is a regulator of insulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of adipocytes, which is essential for whole-body glucose homeostasis. We establish SEC16A as a novel RAB10 effector in this process. Colocalization of SEC16A with RAB10 is augmented by insulin stimulation, and SEC16A knockdown attenuates insulin-induced GLUT4 translocation, phenocopying RAB10 knockdown. We show that SEC16A and RAB10 promote insulin-stimulated mobilization of GLUT4 from a perinuclear recycling endosome/TGN compartment. We propose RAB10-SEC16A functions to accelerate formation of the vesicles that ferry GLUT4 to the PM during insulin stimulation. Because GLUT4 continually cycles between the PM and intracellular compartments, the maintenance of elevated cell-surface GLUT4 in the presence of insulin requires accelerated biogenesis of the specialized GLUT4 transport vesicles. The function of SEC16A in GLUT4 trafficking is independent of its previously characterized activity in ER exit site formation and therefore independent of canonical COPII-coated vesicle function. However, our data support a role for SEC23A, but not the other COPII components SEC13, SEC23B, and SEC31, in the insulin stimulation of GLUT4 trafficking, suggesting that vesicles derived from subcomplexes of COPII coat proteins have a role in the specialized trafficking of GLUT4.
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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.