Evidence map›Paper›PMID 22130660›Full record

ArticleThe Journal of biological chemistry2012

A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis.

Norbert Weiss, Shahid Hameed, José M Fernández-Fernández, Katell Fablet, Maria Karmazinova, Cathy Poillot, Juliane Proft, Lina Chen, Isabelle Bidaud, Arnaud Monteil and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

73 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Activation of GABA transmission by clonazepam reverses the autistic-like phenotypes of the Cav3.2 knockout mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  3. Review
  4. The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Electrophysiological characterization of a CaPflugers Archiv : European journal of physiology · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. CaJournal of thrombosis and haemostasis : JTH · 2022
    Article
  13. Article
  14. Review
  15. Regulation of CaPflugers Archiv : European journal of physiology · 2022
    Article
  16. CaInternational journal of molecular sciences · 2022
    Review
  17. Contribution ofFrontiers in psychiatry · 2022
    Article
  18. Targeting T-type/CaV3.2 channels for chronic pain.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  19. Article
  20. Article

13 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

15 authors at 5 institutions in 4 countries.

Norbert WeissDepartment of Physiology and Pharmacology, Hotchkiss Brain Institute, University of Calgary, Calgary T2N4N1, Canada.
Shahid Hameed
José M Fernández-Fernández
Katell Fablet
Maria Karmazinova
Cathy Poillot
Juliane Proft
Lina Chen
Isabelle Bidaud
Arnaud Monteil
Sylvaine Huc-Brandt
Lubica Lacinova
Philippe Lory
Gerald W Zamponi
Michel De Waard
Centre National de la Recherche Scientifique · FRInserm · FRUniversity of Calgary · CASlovak Academy of Sciences · SKUniversitat Pompeu Fabra · ES

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

T-type calcium channels represent a key pathway for Ca(2+) entry near the resting membrane potential. Increasing evidence supports a unique role of these channels in fast and low-threshold exocytosis in an action potential-independent manner, but the underlying molecular mechanisms have remained unknown. Here, we report the existence of a syntaxin-1A/Ca(v)3.2 T-type calcium channel signaling complex that relies on molecular determinants that are distinct from the synaptic protein interaction site (synprint) found in synaptic high voltage-activated calcium channels. This interaction potently modulated Ca(v)3.2 channel activity, by reducing channel availability. Other members of the T-type calcium channel family were also regulated by syntaxin-1A, but to a smaller extent. Overexpression of Ca(v)3.2 channels in MPC 9/3L-AH chromaffin cells induced low-threshold secretion that could be prevented by uncoupling the channels from syntaxin-1A. Altogether, our findings provide compelling evidence for the existence of a syntaxin-1A/T-type Ca(2+) channel signaling complex and provide new insights into the molecular mechanism by which these channels control low-threshold exocytosis.

Indexed as

Calcium Channels, T-TypeCell LineExocytosisHumansMultiprotein ComplexesSignal TransductionSyntaxin 1CACNA1H protein, humanCalcium Channels, T-TypeMultiprotein ComplexesSyntaxin 1

Identifiers

PMID22130660
PMCPMC3268438
OpenAlexW2110195051

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.