ArticleJournal of lipid research2012
Insulin and AMPK regulate FA translocase/CD36 plasma membrane recruitment in cardiomyocytes via Rab GAP AS160 and Rab8a Rab GTPase.
Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- Baicalin and its aglycone: a novel approach for treatment of metabolic disorders.Pharmacological reports : PR · 2020Pooled it
- Nx3 Is a Z-Disk Structural and Signaling Hub That Is Reduced in Heart Failure.Circulation research · 2026Article
- CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026Review
- Intestinal stearoyl-CoA desaturase-2 is highly expressed and nutritionally regulated but dispensable for energy balance.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026Article
- Moving the fat: Emerging roles of rab GTPases in the regulation of lipid droplet contact sites.Current opinion in cell biology · 2025Review
- Novel Molecules Targeting Metabolism and Mitochondrial Function in Cardiac Diseases.Current cardiology reviews · 2025Review
- Modulation of lipid metabolism by exercise: exploring its potential as a therapeutic target in cancer endocrinology.Frontiers in endocrinology · 2025Review
- AS160 is a lipid-responsive regulator of cardiac CaNature communications · 2024Article
- Insights into Alkaline Phosphatase Anti-Inflammatory Mechanisms.Biomedicines · 2024Review
- Growth Signaling Networks Orchestrate Cancer Metabolic Networks.Cold Spring Harbor perspectives in medicine · 2024Review
- TBC1D1 is an energy-responsive polarization regulator of macrophages via governing ROS production in obesity.Science China. Life sciences · 2024Article
- Hidden features: CD36/SR-B2, a master regulator of macrophage phenotype/function through metabolism.Frontiers in immunology · 2024Review
- Molecular mechanisms of metabolic dysregulation in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2024Review
- Post-translational palmitoylation of metabolic proteins.Frontiers in physiology · 2023Review
- RabGAP AS160/TBC1D4 deficiency increases long-chain fatty acid transport but has little additional effect on obesity and metabolic syndrome in ADMSCs-derived adipocytes of morbidly obese women.Frontiers in molecular biosciences · 2023Article
- Chi-Circ_0006511 Positively Regulates the Differentiation of Goat Intramuscular Adipocytes via Novel-miR-87/CD36 Axis.International journal of molecular sciences · 2022Article
- Article
- The insulin receptor family in the heart: new light on old insights.Bioscience reports · 2022Review
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- Chemotherapy and Physical Therapeutics Modulate Antigens on Cancer Cells.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The FA translocase cluster of differentiation 36 (CD36) facilitates FA uptake by the myocardium, and its surface recruitment in cardiomyocytes is induced by insulin, AMP-dependent protein kinase (AMPK), or contraction. Dysfunction of CD36 trafficking contributes to disordered cardiac FA utilization and promotes progression to disease. The Akt substrate 160 (AS160) Rab GTPase-activating protein (GAP) is a key regulator of vesicular trafficking, and its activity is modulated via phosphorylation. Our study documents that AS160 mediates insulin or AMPK-stimulated surface translocation of CD36 in cardiomyocytes. Knock-down of AS160 redistributes CD36 to the surface and abrogates its translocation by insulin or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR). Conversely, overexpression of a phosphorylation-deficient AS160 mutant (AS160 4P) suppresses the stimulated membrane recruitment of CD36. The AS160 substrate Rab8a GTPase is shown via overexpression and knock-down studies to be specifically involved in insulin/AICAR-induced CD36 membrane recruitment. Our findings directly demonstrate AS160 regulation of CD36 trafficking. In myocytes, the AS160 pathway also mediates the effect of insulin, AMPK, or contraction on surface recruitment of the glucose transporter GLUT4. Thus, AS160 constitutes a point of convergence for coordinating physiological regulation of CD36 and GLUT4 membrane recruitment.
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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.