Evidence map›Paper›PMID 27444020›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

N-terminal domain of complexin independently activates calcium-triggered fusion.

Ying Lai, Ucheor B Choi, Yunxiang Zhang, Minglei Zhao, Richard A Pfuetzner, Austin L Wang, Jiajie Diao, Axel T Brunger

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Molecular Dynamics Simulation for Membrane Fusion.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024
    Article
  10. Mutations of Single Residues in the Complexin N-terminus Exhibit Distinct Phenotypes in Synaptic Vesicle Fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  11. Article
  12. Article
  13. Neutral lysophosphatidylcholine mediates α-synuclein-induced synaptic vesicle clustering.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

8 authors.

Ying LaiDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Ucheor B ChoiDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Yunxiang ZhangDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Minglei ZhaoDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Richard A PfuetznerDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Austin L WangDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304.
Jiajie DiaoDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304 brunger@stanford.edu diaojj@gmail.com.ORCID 0000-0003-4288-3203
Axel T BrungerDepartment of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94304; Department of Structural Biology, Stanford University, Stanford, CA 94304; Department of Photon Science, Stanford University, Stanford, CA 94304; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94304 brunger@stanford.edu diaojj@gmail.com.

Funding

Single molecule studies of SNARE-induced vesicle fusionR37MH063105 · NIMH · STANFORD UNIVERSITY · PI BRUNGER, AXEL T · 2011 to 2020
$4.7M
NIMH NIH HHS R37 MH063105
6 · The paper itself

Abstract

Complexin activates Ca(2+)-triggered neurotransmitter release and regulates spontaneous release in the presynaptic terminal by cooperating with the neuronal soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) and the Ca(2+)-sensor synaptotagmin. The N-terminal domain of complexin is important for activation, but its molecular mechanism is still poorly understood. Here, we observed that a split pair of N-terminal and central domain fragments of complexin is sufficient to activate Ca(2+)-triggered release using a reconstituted single-vesicle fusion assay, suggesting that the N-terminal domain acts as an independent module within the synaptic fusion machinery. The N-terminal domain can also interact independently with membranes, which is enhanced by a cooperative interaction with the neuronal SNARE complex. We show by mutagenesis that membrane binding of the N-terminal domain is essential for activation of Ca(2+)-triggered fusion. Consistent with the membrane-binding property, the N-terminal domain can be substituted by the influenza virus hemagglutinin fusion peptide, and this chimera also activates Ca(2+)-triggered fusion. Membrane binding of the N-terminal domain of complexin therefore cooperates with the other fusogenic elements of the synaptic fusion machinery during Ca(2+)-triggered release.

Indexed as

Membrane FusionAdaptor Proteins, Vesicular TransportCalciumHumansProtein DomainsSNARE ProteinsSynaptic VesiclesSynaptotagmin IAdaptor Proteins, Vesicular TransportCalciumSNARE ProteinsSynaptotagmin Imembrane fusionSNAREssynaptic vesicle fusionsynaptotagminvirus fusion

Identifiers

PMID27444020
PMCPMC4987820

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.