Evidence map›Paper›PMID 24901433›Full record

ArticlePloS one2014

Src kinases regulate de novo actin polymerization during exocytosis in neuroendocrine chromaffin cells.

María José Olivares, Arlek M González-Jamett, María José Guerra, Ximena Baez-Matus, Valentina Haro-Acuña, Narcisa Martínez-Quiles, Ana M Cárdenas

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Multiple Roles of Actin in Exo- and Endocytosis.Frontiers in synaptic neuroscience · 2022
    Review
  6. Anesthetic Propofol Promotes Tumor Metastasis in Lungs via GABAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. 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

7 authors at 2 institutions in 2 countries.

María José OlivaresCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
Arlek M González-JamettCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
María José GuerraCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
Ximena Baez-MatusCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
Valentina Haro-AcuñaCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
Narcisa Martínez-QuilesDepartamento de Microbiología (Inmunología), Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Ana M CárdenasCentro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Playa Ancha, Valparaíso, Chile.
University of Valparaíso · CLUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cortical actin network is dynamically rearranged during secretory processes. Nevertheless, it is unclear how de novo actin polymerization and the disruption of the preexisting actin network control transmitter release. Here we show that in bovine adrenal chromaffin cells, both formation of new actin filaments and disruption of the preexisting cortical actin network are induced by Ca2+ concentrations that trigger exocytosis. These two processes appear to regulate different stages of exocytosis; whereas the inhibition of actin polymerization with the N-WASP inhibitor wiskostatin restricts fusion pore expansion, thus limiting the release of transmitters, the disruption of the cortical actin network with cytochalasin D increases the amount of transmitter released per event. Further, the Src kinase inhibitor PP2, and cSrc SH2 and SH3 domains also suppress Ca2+-dependent actin polymerization, and slow down fusion pore expansion without disturbing the cortical F-actin organization. Finally, the isolated SH3 domain of c-Src prevents both the disruption of the actin network and the increase in the quantal release induced by cytochalasin D. These findings support a model where a rise in the cytosolic Ca2+ triggers actin polymerization through a mechanism that involves Src kinases. The newly formed actin filaments would speed up the expansion of the initial fusion pore, whereas the preexisting actin network might control a different step of the exocytosis process.

Indexed as

Actin CytoskeletonActinsAnimalsCalciumCattleCells, CulturedChromaffin CellsCytochalasin DExocytosisKineticsPyrazolesPyrimidinessrc-Family KinasesWiskott-Aldrich Syndrome Protein, Neuronal4-amino-7-phenylpyrazol(3,4-d)pyrimidineActinsAG 1879CalciumCytochalasin DPyrazolesPyrimidinessrc-Family KinasesWiskott-Aldrich Syndrome Protein, Neuronal

Identifiers

PMID24901433
PMCPMC4047038
OpenAlexW2039645197

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.