Evidence map›Paper›PMID 23401610›Full record

ArticleThe Journal of physiology2013

Complexin facilitates exocytosis and synchronizes vesicle release in two secretory model systems.

Ming-Yi Lin, Joyce G Rohan, Haijiang Cai, Kerstin Reim, Chien-Ping Ko, Robert H Chow

Abstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
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  5. Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Cell-Specific Deletion of PGC-1α from Medium Spiny Neurons Causes Transcriptional Alterations and Age-Related Motor Impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  16. How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018
    Review
  17. Depressed Synaptic Transmission and Reduced Vesicle Release Sites in Huntington's Disease Neuromuscular Junctions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  18. Article
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  20. Review
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

6 authors.

Ming-Yi LinSection of Neurobiology, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089-2520, USA.
Joyce G Rohan
Haijiang Cai
Kerstin Reim
Chien-Ping Ko
Robert H Chow

Funding

MOLECULAR CONTROL OF REGULATED EXOCYTOSISR01GM085791 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHOW, ROBERT HSIU-PING · 2008 to 2011
$1.5M
Insulin granule dynamics in pancreatic beta cellsR01DK060623 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHOW, ROBERT HSIU-PING · 2002 to 2005
$1.1M
Synapse Loss in Spinal Muscular AtrophyR21NS063296 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KO, CHIEN-PING · 2009 to 2010
$390k
Directed differentiation of human embryonic stem cells into glucose-responsive beK18DK091445 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHOW, ROBERT HSIU-PING · 2011 to 2011
$153k
Imaging the Primed Vesicle Pool: A Novel Tool to Study Vesicle PrimingF32GM088967 · NIGMS · WRIGHT STATE UNIVERSITY · PI ROHAN, JOYCE GO · 2009 to 2011
$152k
NIDDK NIH HHS DK60623NIDDK NIH HHS K18 DK091445NIDDK NIH HHS K18DK091445NIDDK NIH HHS R01 DK060623NIGMS NIH HHS F32 GM088967NIGMS NIH HHS F32GM088967NIGMS NIH HHS GM85791NIGMS NIH HHS R01 GM085791NINDS NIH HHS NS063296NINDS NIH HHS R21 NS063296
6 · The paper itself

Abstract

Complexins (Cplxs) are small, SNARE-associated proteins believed to regulate fast, calcium-triggered exocytosis. However, studies have pointed to either an inhibitory and/or facilitatory role in exocytosis, and the role of Cplxs in synchronizing exocytosis is relatively unexplored. Here, we compare the function of two types of complexin, Cplx 1 and 2, in two model systems of calcium-dependent exocytosis. In mouse neuromuscular junctions (NMJs), we find that lack of Cplx 1 significantly reduces and desynchronizes calcium-triggered synaptic transmission; furthermore, high-frequency stimulation elicits synaptic facilitation, instead of normal synaptic depression, and the degree of facilitation is highly sensitive to the amount of cytoplasmic calcium buffering. In Cplx 2-null adrenal chromaffin cells, we also find decreased and desynchronized evoked release, and identify a significant reduction in the vesicle pool close to the calcium channels (immediately releasable pool, IRP). Viral transduction with either Cplx 1 or 2 rescues both the size of the evoked response and the synchronicity of release, and it restores the IRP size. Our findings in two model systems are mutually compatible and indicate a role of Cplx 1 and 2 in facilitating vesicle priming, and also lead to the new hypothesis that Cplxs may synchronize vesicle release by promoting coupling between secretory vesicles and calcium channels.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsCalcium ChannelsChromaffin CellsExocytosisHEK293 CellsHumansIn Vitro TechniquesMiceMice, TransgenicMuscle, SkeletalNerve Tissue ProteinsNeuromuscular JunctionSecretory VesiclesSynapsesAdaptor Proteins, Vesicular TransportCalcium Channelscomplexin Icomplexin IINerve Tissue Proteins

Identifiers

PMID23401610
PMCPMC3678037

What OpenQuestion holds

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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.