Loss of AS160 Akt Substrate Causes Glut4 Protein to Accumulate in Compartments That Are Primed for Fusion in Basal Adipocytes
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference43 articles.
1. Chapter 10 How Insulin Regulates Glucose Transport in Adipocytes
2. Insulin Stimulates the Entry of GLUT4 into the Endosomal Recycling Pathway by a Quantal Mechanism
3. Insulin Increases Cell Surface GLUT4 Levels by Dose Dependently Discharging GLUT4 into a Cell Surface Recycling Pathway
4. Insulin Releases Glut4 from Static Storage Compartments into Cycling Endosomes and Increases the Rate Constant for Glut4 Exocytosis
5. Kinetic Evidence That Glut4 Follows Different Endocytic Pathways than the Receptors for Transferrin and α2-Macroglobulin
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1. Phosphorylation of the N-terminus of Syntaxin-16 controls interaction with mVps45 and GLUT4 trafficking in adipocytes;PeerJ;2023-07-24
2. Olive Leaf Extract of Olea europaea Reduces Blood Glucose Level through Inhibition of AS160 in Diabetic Rats;Applied Sciences;2023-05-11
3. Normalization of maternal adiponectin in obese pregnant mice prevents programming of impaired glucose metabolism in adult offspring;The FASEB Journal;2022-06-07
4. Three live-imaging techniques for comprehensively understanding the initial trigger for insulin-responsive intracellular GLUT4 trafficking;iScience;2022-04
5. GLUT4 On the move;Biochemical Journal;2022-02-11
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