ArticleThe Journal of cell biology1995
Molecular regulation of GLUT-4 targeting in 3T3-L1 adipocytes.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Dynamin2 functions as an accessory protein to reduce the rate of caveola internalization.The Journal of cell biology · 2023Article
- A high-content endogenous GLUT4 trafficking assay reveals new aspects of adipocyte biology.Life science alliance · 2023Article
- Structure, function and regulation of mammalian glucose transporters of the SLC2 family.Pflugers Archiv : European journal of physiology · 2020Review
- Bilobalide Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway.Molecules (Basel, Switzerland) · 2019Article
- Molecular Characterization ofInternational journal of molecular sciences · 2019Article
- Three distinct motifs within the C-terminus of acid-sensing ion channel 1a regulate its surface trafficking.Neuroscience · 2013Article
- Single point mutations result in the miss-sorting of Glut4 to a novel membrane compartment associated with stress granule proteins.PloS one · 2013Article
- Negative regulation of AMP-activated protein kinase (AMPK) activity by macrophage migration inhibitory factor (MIF) family members in non-small cell lung carcinomas.The Journal of biological chemistry · 2012Article
- TBC1D13 is a RAB35 specific GAP that plays an important role in GLUT4 trafficking in adipocytes.Traffic (Copenhagen, Denmark) · 2012Article
- The C-terminus of GLUT4 targets the transporter to the perinuclear compartment but not to the insulin-responsive vesicles.The Biochemical journal · 2009Article
- Molecular mechanisms controlling GLUT4 intracellular retention.Molecular biology of the cell · 2008Article
- Identification of amino acid residues within the C terminus of the Glut4 glucose transporter that are essential for insulin-stimulated redistribution to the plasma membrane.The Journal of biological chemistry · 2008Article
- p115 Interacts with the GLUT4 vesicle protein, IRAP, and plays a critical role in insulin-stimulated GLUT4 translocation.Molecular biology of the cell · 2005Article
- Insulin increases cell surface GLUT4 levels by dose dependently discharging GLUT4 into a cell surface recycling pathway.Molecular and cellular biology · 2004Article
- Insulin stimulates movement of sorting nexin 9 between cellular compartments: a putative role mediating cell surface receptor expression and insulin action.The Biochemical journal · 2003Article
- GLUT4 recycles via a trans-Golgi network (TGN) subdomain enriched in Syntaxins 6 and 16 but not TGN38: involvement of an acidic targeting motif.Molecular biology of the cell · 2003Article
- The NH(2)-terminus of norepinephrine transporter contains a basolateral localization signal for epithelial cells.Molecular biology of the cell · 2001Article
- Insulin-responsive compartments containing GLUT4 in 3T3-L1 and CHO cells: regulation by amino acid concentrations.Molecular and cellular biology · 2001Article
- Insulin resistance and the disruption of Glut4 trafficking in skeletal muscle.The Journal of clinical investigation · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin stimulates glucose transport in muscle and adipose tissue by triggering the movement of the glucose transporter GLUT-4 from an intracellular compartment to the cell surface. Fundamental to this process is the intracellular sequestration of GLUT-4 in nonstimulated cells. Two distinct targeting motifs in the amino and carboxy termini of GLUT-4 have been previously identified by expressing chimeras comprised of portions of GLUT-4 and GLUT-1, a transporter isoform that is constitutively targeted to the cell surface, in heterologous cells. These motifs-FQQI in the NH2 terminus and LL in the COOH terminus-resemble endocytic signals that have been described in other proteins. In the present study we have investigated the roles of these motifs in GLUT-4 targeting in insulin-sensitive cells. Epitope-tagged GLUT-4 constructs engineered to differentiate between endogenous and transfected GLUT-4 were stably expressed in 3T3-L1 adipocytes. Targeting was assessed in cells incubated in the presence or absence of insulin by subcellular fractionation. The targeting of epitope-tagged GLUT-4 was indistinguishable from endogenous GLUT-4. Mutation of the FQQI motif (F5 to A5) caused GLUT-4 to constitutively accumulate at the cell surface regardless of expression level. Mutation of the dileucine motif (L489L490 to A489A490) caused an increase in cell surface distribution only at higher levels of expression, but the overall cells surface distribution of this mutant was less than that of the amino-terminal mutants. Both NH2- and COOH-terminal mutants retained insulin-dependent movement from an intracellular to a cell surface locale, suggesting that neither of these motifs is involved in the insulin-dependent redistribution of GLUT-4. We conclude that the phenylalanine-based NH2-terminal and the dileucine-based COOH-terminal motifs play important and distinct roles in GLUT-4 targeting in 3T3-L1 adipocytes.
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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.