Evidence map›Paper›PMID 11438680›Full record

ArticleMolecular and cellular biology2001

G(alpha)11 signaling through ARF6 regulates F-actin mobilization and GLUT4 glucose transporter translocation to the plasma membrane.

A Bose, A D Cherniack, S E Langille, S M Nicoloro, J M Buxton, J G Park, A Chawla, M P Czech

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. S6 Kinase Reflects and Regulates Ethanol-Induced Sedation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  6. Article
  7. Article
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  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Control of dendritic arborization by the phosphoinositide-3'-kinase-Akt-mammalian target of rapamycin pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Fluidity of insulin action.Molecular biotechnology · 2004
    Review
  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

8 authors at 1 institution in 2 countries.

A BoseProgram in Molecular Medicine and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical Center, Worcester, Massachusetts 01605, USA.
A D Cherniack
S E Langille
S M Nicoloro
J M Buxton
J G Park
A Chawla
M P Czech
University of Massachusetts Chan Medical School · US

Funding

PROPERTIES OF THE HIGH-AFFINITY INSULIN RECEPTORR01DK030648 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2008
$3.6M
NIDDK NIH HHS DK30648NIDDK NIH HHS R01 DK030648
6 · The paper itself

Abstract

The action of insulin to recruit the intracellular GLUT4 glucose transporter to the plasma membrane of 3T3-L1 adipocytes is mimicked by endothelin 1, which signals through trimeric G(alpha)q or G(alpha)11 proteins. Here we report that murine G(alpha)11 is most abundant in fat and that expression of the constitutively active form of G(alpha)11 [G(alpha)11(Q209L)] in 3T3-L1 adipocytes causes recruitment of GLUT4 to the plasma membrane and stimulation of 2-deoxyglucose uptake. In contrast to the action of insulin on GLUT4, the effects of endothelin 1 and G(alpha)11 were not inhibited by the phosphatidylinositol 3-kinase inhibitor wortmannin at 100 nM. Signaling by insulin, endothelin 1, or G(alpha)11(Q209L) also mobilized cortical F-actin in cultured adipocytes. Importantly, GLUT4 translocation caused by all three agents was blocked upon disassembly of F-actin by latrunculin B, suggesting that the F-actin polymerization caused by these agents may be required for their effects on GLUT4. Remarkably, expression of a dominant inhibitory form of the actin-regulatory GTPase ARF6 [ARF6(T27N)] in cultured adipocytes selectively inhibited both F-actin formation and GLUT4 translocation in response to endothelin 1 but not insulin. These data indicate that ARF6 is a required downstream element in endothelin 1 signaling through G(alpha)11 to regulate cortical actin and GLUT4 translocation in cultured adipocytes, while insulin action involves different signaling pathways.

Indexed as

Muscle ProteinsSignal TransductionActinsAdenoviridaeAdipocytesADP-Ribosylation Factor 6ADP-Ribosylation FactorsAndrostadienesAnimalsAntimetabolitesAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCell LineCell MembraneCells, CulturedDeoxyglucoseActinsADP-Ribosylation Factor 6ADP-Ribosylation FactorsAndrostadienesAntimetabolitesAntineoplastic AgentsArf6 protein, mouseArf6 protein, ratBridged Bicyclo Compounds, HeterocyclicDeoxyglucoseEndothelin-1Enzyme InhibitorsGlucose Transporter Type 4GTP-Binding Protein alpha Subunits, Gq-G11Heterotrimeric GTP-Binding ProteinsInsulinlatrunculin BMonosaccharide Transport ProteinsMuscle ProteinsNocodazolePhosphoinositide-3 Kinase InhibitorsSlc2a4 protein, mouseSlc2a4 protein, ratThiazolesThiazolidinesWortmannin

Identifiers

PMID11438680
PMCPMC87250
OpenAlexW2118361286

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.