Evidence map›Paper›PMID 17139247›Full record

ArticleThe EMBO journal2006

GLUT4 is internalized by a cholesterol-dependent nystatin-sensitive mechanism inhibited by insulin.

Vincent Blot, Timothy E McGraw

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. GLUT4 On the move.The Biochemical journal · 2022
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019
    Review
  17. Article
  18. Insulin differentially affects the distribution kinetics of amyloid beta 40 and 42 in plasma and brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  19. Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Vincent BlotDepartment of Biochemistry, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA.
Timothy E McGraw
Cornell University · US

Funding

Endocytic Trafficking Pathways in AdipocytesR01DK069982 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MCGRAW, TIMOTHY E · 2006 to 2009
$1.3M
Endocytic Trafficking Pathways in AdipocytesR56DK069982 · NIDDK · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MCGRAW, TIMOTHY E · 2005 to 2005
$126k
NIDDK NIH HHS DK 69982NIDDK NIH HHS R01 DK069982NIDDK NIH HHS R56 DK069982
6 · The paper itself

Abstract

Insulin slows GLUT4 internalization by an unknown mechanism. Here we show that in unstimulated adipocytes, GLUT4 is internalized by two mechanisms. Approximately 80% of GLUT4 is internalized by a mechanism that is sensitive to the cholesterol-aggregating drug nystatin, and is independent of AP-2 clathrin adaptor and two putative GLUT4 endocytic motifs. The remaining GLUT4 is internalized by an AP-2-dependent, nystatin-resistant pathway that requires the FQQI GLUT4 motif. Insulin inhibits GLUT4 uptake by the nystatin-sensitive pathway and, consequently, GLUT4 is internalized by the AP-2-dependent pathway in stimulated adipocytes. The phenylalanine-based FQQI GLUT4 motif promotes AP-2-dependent internalization less rapidly than a tyrosine-based motif, the classic form of aromatic-based motifs. Thus, both a change in the predominant endocytosis pathway and the specific use of a suboptimal internalization motif contribute to the slowing of GLUT4 internalization in insulin-stimulated adipocytes. Insulin also inhibits the uptake of cholera-toxin B, indicating that insulin broadly regulates cholesterol-dependent uptake mechanisms rather than specially targeting GLUT4. Our work thus identifies cholesterol-dependent uptake as a novel target of insulin action in adipocytes.

Indexed as

3T3-L1 CellsAdaptor Protein Complex 2AdipocytesAmino Acid MotifsAmino Acid SequenceAnimalsCholesterolEndocytosisGlucose Transporter Type 4HumansInsulinMiceModels, BiologicalMolecular Sequence DataMutagenesisMutant ProteinsAdaptor Protein Complex 2CholesterolGlucose Transporter Type 4InsulinMutant ProteinsNystatinTransferrin

Identifiers

PMID17139247
PMCPMC1698906
OpenAlexW2113580156

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.