Evidence map›Paper›PMID 14595108›Full record

ArticleMolecular biology of the cell2004

GLUT4 is retained by an intracellular cycle of vesicle formation and fusion with endosomes.

Ola Karylowski, Anja Zeigerer, Alona Cohen, Timothy E McGraw

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

79 citing papers in PubMed, 182 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Genetic marker identification ofFrontiers in genetics · 2022
    Article
  12. Microtubules in insulin action: what's on the tube?Trends in endocrinology and metabolism: TEM · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019
    Review
  19. Article
  20. The cell biology of systemic insulin function.The Journal of cell biology · 2018
    Review

19 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Ola KarylowskiDepartment of Biochemistry, and Program in Biochemistry and Structural Biology, Weill Medical College of Cornell University, New York, New York 10021, USA.
Anja Zeigerer
Alona Cohen
Timothy E McGraw
Cornell University · US

Funding

INSULIN REGULATED MEMBRANE TRAFFICKINGR01DK052852 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MCGRAW, TIMOTHY E · 1997 to 2016
$6.1M
REGULATED ENDOCYTIC TRAFFIC IN FIBROBLASTSR01DK057689 · NIDDK · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MCGRAW, TIMOTHY E · 2001 to 2004
$1.2M
Insulin Regulated Membrane TraffickingR56DK052852 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MCGRAW, TIMOTHY E · 2017 to 2017
$254k
NIDDK NIH HHS DK52852NIDDK NIH HHS DK57689NIDDK NIH HHS R01 DK052852NIDDK NIH HHS R01 DK057689
6 · The paper itself

Abstract

The intracellularly stored GLUT4 glucose transporter is rapidly translocated to the cell surface upon insulin stimulation. Regulation of GLUT4 distribution is key for the maintenance of whole body glucose homeostasis. We find that GLUT4 is excluded from the plasma membrane of adipocytes by a dynamic retention/retrieval mechanism. Our kinetic studies indicate that GLUT4-containing vesicles continually bud and fuse with endosomes in the absence of insulin and that these GLUT4 vesicles are 5 times as likely to fuse with an endosome as with the plasma membrane. We hypothesize that this intracellular cycle of vesicle budding and fusion is an element of the active mechanism by which GLUT4 is retained. The GLUT4 trafficking pathway does not extensively overlap with that of furin, indicating that the trans-Golgi network, a compartment in which furin accumulates, is not a significant storage reservoir of GLUT4. An intact microtubule cytoskeleton is required for insulin-stimulated recruitment to the cell surface, although it is not required for the basal budding/fusion cycle. Nocodazole disruption of the microtubule cytoskeleton reduces the insulin-stimulated exocytosis of GLUT4, accounting for the reduced insulin-stimulated translocation of GLUT4 to the cell surface.

Indexed as

3T3-L1 CellsAdipocytesAnimalsBiological TransportCell DifferentiationCell MembraneCytoskeletonEndosomesExocytosisGlucoseGlucose Transporter Type 4InsulinMiceMicrotubulesMonosaccharide Transport ProteinsMuscle ProteinsGlucoseGlucose Transporter Type 4InsulinMonosaccharide Transport ProteinsMuscle ProteinsNocodazoleSlc2a4 protein, mouse

Identifiers

PMID14595108
PMCPMC329400
OpenAlexW2117239289

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.