Evidence map›Paper›PMID 24274740›Full record

ReviewAnnual review of physiology2014

Exocytosis and endocytosis: modes, functions, and coupling mechanisms.

Ling-Gang Wu, Edaeni Hamid, Wonchul Shin, Hsueh-Cheng Chiang

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed
12.6field-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

234 citing papers in PubMed, 455 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. BLOC1S1 regulates autolysosomal and exosomal dynamics during CD4bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Membrane Merger Dynamics in Exocytosis and Endocytosis.Advances in experimental medicine and biology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Fusion Pores as Regulators of Quantal Size and Cellular Physiology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

174 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.

Ling-Gang WuNational Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892; email: wul@ninds.nih.gov , edaeni.hamid@nih.gov.
Edaeni Hamid
Wonchul Shin
Hsueh-Cheng Chiang
National Institute of Neurological Disorders and Stroke · US

Funding

Synaptic Vesicle ExocytosisZIANS003009 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WU, LING GANG · 2009 to 2025
$31.2M
Synaptic Vesicle EndocytosisZIANS003105 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WU, LING GANG · 2009 to 2025
$30.9M
Synaptic Vesicle Exocytosis and EndocytosisZ01NS003009 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI WU, LING GANG · 2004 to 2008
$4.9M
Intramural NIH HHS Z01 NS003009
6 · The paper itself

Abstract

Vesicle exocytosis releases content to mediate many biological events, including synaptic transmission essential for brain functions. Following exocytosis, endocytosis is initiated to retrieve exocytosed vesicles within seconds to minutes. Decades of studies in secretory cells reveal three exocytosis modes coupled to three endocytosis modes: (a) full-collapse fusion, in which vesicles collapse into the plasma membrane, followed by classical endocytosis involving membrane invagination and vesicle reformation; (b) kiss-and-run, in which the fusion pore opens and closes; and (c) compound exocytosis, which involves exocytosis of giant vesicles formed via vesicle-vesicle fusion, followed by bulk endocytosis that retrieves giant vesicles. Here we review these exo- and endocytosis modes and their roles in regulating quantal size and synaptic strength, generating synaptic plasticity, maintaining exocytosis, and clearing release sites for vesicle replenishment. Furthermore, we highlight recent progress in understanding how vesicle endocytosis is initiated and is thus coupled to exocytosis. The emerging model is that calcium influx via voltage-dependent calcium channels at the calcium microdomain triggers endocytosis and controls endocytosis rate; calmodulin and synaptotagmin are the calcium sensors; and the exocytosis machinery, including SNARE proteins (synaptobrevin, SNAP25, and syntaxin), is needed to coinitiate endocytosis, likely to control the amount of endocytosis.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingCalmodulinCell MembraneEndocytosisExocytosisHumansNeuronal PlasticitySynaptic VesiclesSynaptotagminsCalciumCalcium ChannelsCalmodulinSynaptotagmins

Identifiers

PMID24274740
PMCPMC4880020
OpenAlexW2122968189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.