Evidence map›Paper›PMID 15071120›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Molecular determinants of synapsin targeting to presynaptic terminals.

Daniel Gitler, Yimei Xu, Hung-Teh Kao, Dayu Lin, Sangmi Lim, Jian Feng, Paul Greengard, George J Augustine

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

69 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  15. Synapsin Is Required for Dense Core Vesicle Capture and cAMP-Dependent Neuropeptide Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Functional cooperation of α-synuclein and VAMP2 in synaptic vesicle recycling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

9 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

8 authors at 4 institutions in 1 country.

Daniel GitlerDepartment of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Yimei Xu
Hung-Teh Kao
Dayu Lin
Sangmi Lim
Jian Feng
Paul Greengard
George J Augustine
Duke University Hospital · USRockefeller University · USDuke Medical Center · USDuke University · US

Funding

SYNAPSINS: REGULATORS OF NEUROTRANSMITTER RELEASER01MH039327 · NIMH · ROCKEFELLER UNIVERSITY · PI GREENGARD, PAUL · 1985 to 2006
$2.9M
Transmission at Synapsin-deficient SynapsesR01MH067044 · NIMH · DUKE UNIVERSITY · PI AUGUSTINE, GEORGE J. · 2003 to 2006
$1.2M
SYNAPSINS: REGULATORS OF NEUROTRANSMITTER RELEASER37MH039327 · NIMH · ROCKEFELLER UNIVERSITY · PI GREENGARD, PAUL · 1991 to 2000
$671k
NIMH NIH HHS MH 39327NIMH NIH HHS MH 67044NIMH NIH HHS R01 MH039327NIMH NIH HHS R01 MH067044NIMH NIH HHS R37 MH039327
6 · The paper itself

Abstract

Although synapsins are abundant synaptic vesicle proteins that are widely used as markers of presynaptic terminals, the mechanisms that target synapsins to presynaptic terminals have not been elucidated. We have addressed this question by imaging the targeting of green fluorescent protein-tagged synapsins in cultured hippocampal neurons. Whereas all synapsin isoforms targeted robustly to presynaptic terminals in wild-type neurons, synapsin Ib scarcely targeted in neurons in which all synapsins were knocked-out. Coexpression of other synapsin isoforms significantly strengthened the targeting of synapsin Ib in knock-out neurons, indicating that heterodimerization is required for synapsin Ib to target. Truncation mutagenesis revealed that synapsin Ia targets via distributed binding sites that include domains B, C, and E. Although domain A was not necessary for targeting, its presence enhanced targeting. Domain D inhibited targeting, but this inhibition was overcome by domain E. Thus, multiple intermolecular and intramolecular interactions are required for synapsins to target to presynaptic terminals.

Indexed as

AnimalsCells, CulturedDimerizationGene TargetingGreen Fluorescent ProteinsLuminescent ProteinsMiceMice, KnockoutMutagenesis, Site-DirectedNeuronsPhosphorylationPresynaptic TerminalsProtein IsoformsProtein Structure, TertiaryProtein TransportRecombinant Fusion ProteinsGreen Fluorescent ProteinsLuminescent ProteinsProtein IsoformsRecombinant Fusion ProteinsSynapsins

Identifiers

PMID15071120
PMCPMC6729754
OpenAlexW2121699552

What OpenQuestion holds

Textmetadata
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.