Evidence map›Paper›PMID 7860632›Full record

ArticleThe Journal of cell biology1995

Actin filament disassembly is a sufficient final trigger for exocytosis in nonexcitable cells.

S Muallem, K Kwiatkowska, X Xu, H L Yin

Open access · bronzeAbstract read
In one paragraph

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 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 427 citations in OpenAlex.

  1. Article
  2. Review
  3. Assays of Platelet SNARE-actin Interactions.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Do Animal Models of Acute Pancreatitis Reproduce Human Disease?Cellular and molecular gastroenterology and hepatology · 2017
    Review
  17. Article
  18. Article
  19. Review
  20. Article

73 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.

S MuallemDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas 75235-9040.
K Kwiatkowska
X Xu
H L Yin
The University of Texas Southwestern Medical Center · US

Funding

STRUCTURE/FUNCTION ANALYSIS OF CYTOPLASMIC GELSOLINR01GM051112 · NIGMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI YIN, HELEN L · 1994 to 2003
$1.2M
REGULATION OF NEURONAL ACTIN BY BETA-THYMOSINSR01NS031430 · NINDS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI YIN, HELEN L · 1993 to 1999
–
NIDDK NIH HHS DK32938NIGMS NIH HHS GM51112NINDS NIH HHS NS31430
6 · The paper itself

Abstract

Although the actin cytoskeleton has been implicated in vesicle trafficking, docking and fusion, its site of action and relation to the Ca(2+)-mediated activation of the docking and fusion machinery have not been elucidated. In this study, we examined the role of actin filaments in regulated exocytosis by introducing highly specific actin monomer-binding proteins, the beta-thymosins or a gelsolin fragment, into streptolysin O-permeabilized pancreatic acinar cells. These proteins had stimulatory and inhibitory effects. Low concentrations elicited rapid and robust exocytosis with a profile comparable to the initial phase of regulated exocytosis, but without raising [Ca2+], and even when [Ca2+] was clamped at low levels by EGTA. No additional cofactors were required. Direct visualization and quantitation of actin filaments showed that beta-thymosin, like agonists, induced actin depolymerization at the apical membrane where exocytosis occurs. Blocking actin depolymerization by phalloidin or neutralizing beta-thymosin by complexing with exogenous actin prevented exocytosis. These findings show that the cortical actin network acts as a dominant negative clamp which blocks constitutive exocytosis. In addition, actin filaments also have a positive role. High concentrations of the actin depolymerizing proteins inhibited all phases of exocytosis. The inhibition overrides stimulation by agonists and all downstream effectors tested, suggesting that exocytosis cannot occur without a minimal actin cytoskeletal structure.

Indexed as

ActinsAnimalsCalciumCarbacholCell Membrane PermeabilityCytoskeletonExocytosisGelsolinGuanosine 5'-O-(3-Thiotriphosphate)Inositol 1,4,5-TrisphosphatePancreasPolymersRatsSincalideStreptolysinsTetradecanoylphorbol AcetateActinsCalciumCarbacholGelsolinGuanosine 5'-O-(3-Thiotriphosphate)Inositol 1,4,5-TrisphosphatePolymersSincalideStreptolysinsTetradecanoylphorbol AcetateThymosinthymosin beta(10)

Identifiers

PMID7860632
PMCPMC2199902
OpenAlexW2105630800

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.