Evidence map›Paper›PMID 19675672›Full record

ArticlePloS one2009

Selective interaction of syntaxin 1A with KCNQ2: possible implications for specific modulation of presynaptic activity.

Noa Regev, Nurit Degani-Katzav, Alon Korngreen, Adi Etzioni, Sivan Siloni, Alessandro Alaimo, Dodo Chikvashvili, Alvaro Villarroel, Bernard Attali, Ilana Lotan

Abstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021
    Article
  5. Epileptic channelopathies caused by neuronal Kv7 (KCNQ) channel dysfunction.Pflugers Archiv : European journal of physiology · 2020
    Review
  6. The Role of KFrontiers in physiology · 2020
    Review
  7. Review
  8. Activation of Kv7 Potassium Channels Inhibits Intracellular CaInternational journal of molecular sciences · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Modulation of Kv7 channels and excitability in the brain.Cellular and molecular life sciences : CMLS · 2017
    Review
  13. Distinct Functions of Syntaxin-1 in Neuronal Maintenance, Synaptic Vesicle Docking, and Fusion in Mouse Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  14. Neuronal pentraxin 1 negatively regulates excitatory synapse density and synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. Article
  16. Article
  17. Structural insights into neuronal K+ channel-calmodulin complexes.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. A role for dynamin in triggering ethanol tolerance.Alcoholism, clinical and experimental research · 2012
    Article
  19. Regulation of neuronal M-channel gating in an isoform-specific manner: functional interplay between calmodulin and syntaxin 1A.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  20. Article
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

10 authors.

Noa RegevDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel-Aviv University, Ramat-Aviv, Israel.
Nurit Degani-Katzav
Alon Korngreen
Adi Etzioni
Sivan Siloni
Alessandro Alaimo
Dodo Chikvashvili
Alvaro Villarroel
Bernard Attali
Ilana Lotan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KCNQ2/KCNQ3 channels are the molecular correlates of the neuronal M-channels, which play a major role in the control of neuronal excitability. Notably, they differ from homomeric KCNQ2 channels in their distribution pattern within neurons, with unique expression of KCNQ2 in axons and nerve terminals. Here, combined reciprocal coimmunoprecipitation and two-electrode voltage clamp analyses in Xenopus oocytes revealed a strong association of syntaxin 1A, a major component of the exocytotic SNARE complex, with KCNQ2 homomeric channels resulting in a approximately 2-fold reduction in macroscopic conductance and approximately 2-fold slower activation kinetics. Remarkably, the interaction of KCNQ2/Q3 heteromeric channels with syntaxin 1A was significantly weaker and KCNQ3 homomeric channels were practically resistant to syntaxin 1A. Analysis of different KCNQ2 and KCNQ3 chimeras and deletion mutants combined with in-vitro binding analysis pinpointed a crucial C-terminal syntaxin 1A-association domain in KCNQ2. Pull-down and coimmunoprecipitation analyses in hippocampal and cortical synaptosomes demonstrated a physical interaction of brain KCNQ2 with syntaxin 1A, and confocal immunofluorescence microscopy showed high colocalization of KCNQ2 and syntaxin 1A at presynaptic varicosities. The selective interaction of syntaxin 1A with KCNQ2, combined with a numerical simulation of syntaxin 1A's impact in a firing-neuron model, suggest that syntaxin 1A's interaction is targeted at regulating KCNQ2 channels to fine-tune presynaptic transmitter release, without interfering with the function of KCNQ2/3 channels in neuronal firing frequency adaptation.

Indexed as

AnimalsBlotting, WesternElectrophoresis, Polyacrylamide GelHippocampusImmunohistochemistryKCNQ2 Potassium ChannelOocytesPresynaptic TerminalsProtein BindingSyntaxin 1Xenopus laevisKCNQ2 Potassium ChannelSyntaxin 1

Identifiers

PMID19675672
PMCPMC2721677

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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.