Evidence map›Paper›PMID 23440961›Full record

ArticleThe Journal of physiology2013

Dipeptidyl-peptidase-like-proteins confer high sensitivity to the scorpion toxin AmmTX3 to Kv4-mediated A-type K+ channels.

Jon K Maffie, Elena Dvoretskova, Pierre Edouard Bougis, Marie-France Martin-Eauclaire, Bernardo Rudy

Open access · greenAbstract 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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Long-Term Inactivation of Sodium Channels as a Mechanism of Adaptation in CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  11. Article
  12. Article
  13. R-type voltage-gated CaCell reports · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Effects of bradykinin on voltage-gated KThe Journal of physiology · 2021
    Article
  18. Article
  19. Variation of Two S3b Residues in KFrontiers in pharmacology · 2021
    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

5 authors at 2 institutions in 2 countries.

Jon K MaffieSmilow Neuroscience Program, NYU School of Medicine, 522 First Avenue, New York, NY 10016, USA.
Elena Dvoretskova
Pierre Edouard Bougis
Marie-France Martin-Eauclaire
Bernardo Rudy
Neurosciences Institute · USCentre de Recherche en Neurobiologie - Neurophysiologie de Marseille · FR

Funding

The Role of DPP6 in Kv4 Localization and Dendritic ExcitabilityF30NS071660 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MAFFIE, JONATHON K · 2010 to 2012
$81k
NINDS NIH HHS F30 NS071660NINDS NIH HHS NS04517
6 · The paper itself

Abstract

K+ channels containing Kv4.2 and Kv4.3 pore-forming subunits mediate most of the subthreshold-operating somatodendritic A-type K+ current in CNS neurons. These channels are believed to be important in regulating the frequency of repetitive firing, the backpropagation of action potential into dendrites, and dendritic integration and plasticity. Moreover, they have been implicated in several diseases from pain to epilepsy and autism spectrum disorders. The lack of toxins that specifically and efficiently block these channels has hampered studies aimed at confirming their functional role and their involvement in disease. AmmTX3 and other related members of the α-KTX15 family of scorpion toxins have been shown to block the A-type K+ current in cultured neurons, but their specificity has been questioned because the toxins do not efficiently block the currents mediated by Kv4.2 or Kv4.3 subunits expressed in heterologous cells. Here we show that the high-affinity blockade of Kv4.2 and Kv4.3 channels by AmmTX3 depends on the presence of the auxiliary subunits DPP6 and DPP10. These proteins are thought to be components of the Kv4 channel complex in neurons and to be important for channel expression in dendrites. These studies validate the use of AmmTX3 as a blocker of the Kv4-mediated A-type K+ current in neurons.

Indexed as

AnimalsCells, CulturedCerebellumCHO CellsCricetinaeCricetulusDipeptidyl-Peptidases and Tripeptidyl-PeptidasesMiceMice, KnockoutNeuronsRecombinant ProteinsScorpion VenomsShal Potassium ChannelsAmmTX3 protein, Androctonus mauretanicusDipeptidyl-Peptidases and Tripeptidyl-PeptidasesDPP6 protein, mouseRecombinant ProteinsScorpion VenomsShal Potassium Channels

Identifiers

PMID23440961
PMCPMC3678034
OpenAlexW1484100077

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.