Characterization of the insulin-regulated endocytic recycling mechanism in 3T3-L1 adipocytes using a novel reporter molecule.
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Intracellular Transport Routes for MHC I and Their Relevance for Antigen Cross-PresentationTankyrase is a golgi-associated mitogen-activated protein kinase substrate that interacts with IRAP in GLUT4 vesiclesMice deficient in the insulin-regulated membrane aminopeptidase show substantial decreases in glucose transporter GLUT4 levels but maintain normal glucose homeostasisp115 Interacts with the GLUT4 vesicle protein, IRAP, and plays a critical role in insulin-stimulated GLUT4 translocationCortactin, an actin binding protein, regulates GLUT4 translocation via actin filament remodelingInsulin-regulated aminopeptidase is a key regulator of GLUT4 trafficking by controlling the sorting of GLUT4 from endosomes to specialized insulin-regulated vesiclesSelf-assembly of Glut4 storage vesicles during differentiation of 3T3-L1 adipocytesInsulin signaling diverges into Akt-dependent and -independent signals to regulate the recruitment/docking and the fusion of GLUT4 vesicles to the plasma membraneDirect quantification of fusion rate reveals a distal role for AS160 in insulin-stimulated fusion of GLUT4 storage vesicles.Identification of a distal GLUT4 trafficking event controlled by actin polymerizationInsulin action on GLUT4 traffic visualized in single 3T3-l1 adipocytes by using ultra-fast microscopy.The GLUT4 codeSecretion of Adipsin as an Assay to Measure Flux from the Endoplasmic Reticulum (ER).Insulin-regulated release from the endosomal recycling compartment is regulated by budding of specialized vesicles.Entry of newly synthesized GLUT4 into the insulin-responsive storage compartment is GGA dependent.A di-leucine sequence and a cluster of acidic amino acids are required for dynamic retention in the endosomal recycling compartment of fibroblasts.Golgin-160 is required for the Golgi membrane sorting of the insulin-responsive glucose transporter GLUT4 in adipocytes.GLUT4 is retained by an intracellular cycle of vesicle formation and fusion with endosomesThe role of insulin-regulated aminopeptidase in MHC class I antigen presentation.Myosin 5a is an insulin-stimulated Akt2 (protein kinase Bbeta) substrate modulating GLUT4 vesicle translocation.Nonclassical, distinct endocytic signals dictate constitutive and PKC-regulated neurotransmitter transporter internalization.SEC16A is a RAB10 effector required for insulin-stimulated GLUT4 trafficking in adipocytes.Insulin stimulation of GLUT4 exocytosis, but not its inhibition of endocytosis, is dependent on RabGAP AS160.The sugar is sIRVed: sorting Glut4 and its fellow travelers.Insulin-responsive compartments containing GLUT4 in 3T3-L1 and CHO cells: regulation by amino acid concentrationsGLUT4 retention in adipocytes requires two intracellular insulin-regulated transport steps.Insulin accelerates inter-endosomal GLUT4 traffic via phosphatidylinositol 3-kinase and protein kinase B.Molecular mechanisms controlling GLUT4 intracellular retention.GLUT4 is internalized by a cholesterol-dependent nystatin-sensitive mechanism inhibited by insulin.Recycling of IRAP from the plasma membrane back to the insulin-responsive compartment requires the Q-SNARE syntaxin 6 but not the GGA clathrin adaptors.Distinct Akt phosphorylation states are required for insulin regulated Glut4 and Glut1-mediated glucose uptake.Initial entry of IRAP into the insulin-responsive storage compartment occurs prior to basal or insulin-stimulated plasma membrane recycling.GLUT4 distribution between the plasma membrane and the intracellular compartments is maintained by an insulin-modulated bipartite dynamic mechanism.A specific dileucine motif is required for the GGA-dependent entry of newly synthesized insulin-responsive aminopeptidase into the insulin-responsive compartment.Microtubule network is required for insulin signaling through activation of Akt/protein kinase B: evidence that insulin stimulates vesicle docking/fusion but not intracellular mobility.Suppression of PPAR-gamma attenuates insulin-stimulated glucose uptake by affecting both GLUT1 and GLUT4 in 3T3-L1 adipocytes.The luminal Vps10p domain of sortilin plays the predominant role in targeting to insulin-responsive Glut4-containing vesicles.
P2860
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P2860
Characterization of the insulin-regulated endocytic recycling mechanism in 3T3-L1 adipocytes using a novel reporter molecule.
description
2000 nî lūn-bûn
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2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Characterization of the insuli ...... ing a novel reporter molecule.
@en
Characterization of the insuli ...... ing a novel reporter molecule.
@nl
type
label
Characterization of the insuli ...... ing a novel reporter molecule.
@en
Characterization of the insuli ...... ing a novel reporter molecule.
@nl
prefLabel
Characterization of the insuli ...... ing a novel reporter molecule.
@en
Characterization of the insuli ...... ing a novel reporter molecule.
@nl
P2093
P2860
P356
P1476
Characterization of the insuli ...... ing a novel reporter molecule.
@en
P2093
P2860
P304
P356
10.1074/JBC.275.7.4787
P407
P577
2000-02-01T00:00:00Z