Evidence map›Paper›PMID 18285343›Full record

ArticleThe Journal of biological chemistry2008

Filamentous actin regulates insulin exocytosis through direct interaction with Syntaxin 4.

Jenna L Jewell, Wei Luo, Eunjin Oh, Zhanxiang Wang, Debbie C Thurmond

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 104 citations in OpenAlex.

  1. Alterations of actin in aging.Journal of cell science · 2026
    Review
  2. Review
  3. Assays of Platelet SNARE-actin Interactions.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  4. Insulin secretion hot spots in pancreatic β cells as secreting adhesions.Frontiers in cell and developmental biology · 2023
    Article
  5. Novel roles of mTORC2 in regulation of insulin secretion by actin filament remodeling.American journal of physiology. Endocrinology and metabolism · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Exocytosis proteins as novel targets for diabetes prevention and/or remediation?American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Review
  20. Review

7 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

5 authors at 3 institutions in 1 country.

Jenna L JewellDepartment of Biochemistry and Molecular Biology, Center for Diabetes Research, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Wei Luo
Eunjin Oh
Zhanxiang Wang
Debbie C Thurmond
Indiana University – Purdue University Indianapolis · USAllscripts (United States) · USIndiana University School of Medicine

Funding

Regulation of Glucose Homeostasis by Munc18 ProteinsR01DK067912 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI THURMOND, DEBBIE C · 2004 to 2023
$6.5M
Cdc42-regulated insulin granule exocytosisR01DK076614 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI THURMOND, DEBBIE C · 2008 to 2012
$1.6M
NIDDK NIH HHS DK-067912NIDDK NIH HHS DK-76614NIDDK NIH HHS R01 DK067912NIDDK NIH HHS R01 DK076614
6 · The paper itself

Abstract

Glucose-induced insulin exocytosis is coupled to associations between F-actin and SNARE proteins, although the nature and function of these interactions remains unknown. Toward this end we show here that both Syntaxin 1A and Syntaxin 4 associated with F-actin in MIN6 cells and that each interaction was rapidly and transiently diminished by stimulation of cells with d-glucose. Of the two isoforms, only Syntaxin 4 was capable of interacting directly with F-actin in an in vitro sedimentation assay, conferred by the N-terminal 39-112 residues of Syntaxin 4. The 39-112 fragment was capable of selective competitive inhibitory action, disrupting endogenous F-actin-Syntaxin 4 binding in MIN6 cells. Disruption of F-actin-Syntaxin 4 binding correlated with enhanced glucose-stimulated insulin secretion, mediated by increased granule accumulation at the plasma membrane and increased Syntaxin 4 accessibility under basal conditions. However, no increase in basal level Syntaxin 4-VAMP2 association occurred with either latrunculin treatment or expression of the 39-112 fragment. Taken together, these data disclose a new underlying mechanism by which F-actin negatively regulates exocytosis via binding and blocking Syntaxin 4 accessibility, but they also reveal the existence of additional signals and/or steps required to trigger the subsequent docking and fusion steps of exocytosis.

Indexed as

ActinsAmino Acid MotifsAnimalsBridged Bicyclo Compounds, HeterocyclicCell LineCell MembraneExocytosisHumansInsulinMiceModels, BiologicalProtein BindingProtein IsoformsQa-SNARE ProteinsRabbitsThiazolidinesActinsBridged Bicyclo Compounds, HeterocyclicInsulinlatrunculin BProtein IsoformsQa-SNARE ProteinsThiazolidines

Identifiers

PMID18285343
PMCPMC2376824
OpenAlexW2012745970

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.