Evidence map›Paper›PMID 23012651›Full record

ReviewToxins2012

Animal toxins can alter the function of Nav1.8 and Nav1.9.

John Gilchrist, Frank Bosmans

Abstract readReview
In one paragraph

Review in Toxins, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Australian ScorpionBiomolecules · 2020
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Animal toxins influence voltage-gated sodium channel function.Handbook of experimental pharmacology · 2014
    Review
  13. Venom: the sharp end of pain therapeutics.British journal of pain · 2013
    Article
  14. Article
  15. Article
  16. 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

2 authors.

John GilchristDepartment of Physiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Frank Bosmans

Funding

The influence of beta-subunits and sphingomyelin on sodium channel functionR00NS073797 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BOSMANS, FRANK GERT WERNER · 2012 to 2014
$730k
NINDS NIH HHS R00 NS073797NINDS NIH HHS R00NS073797
6 · The paper itself

Abstract

Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals across long distances in various excitable tissues. As such, they are amongst the most widely targeted ion channels by drugs and animal toxins. Of the nine isoforms, Nav1.8 and Nav1.9 are preferentially expressed in DRG neurons where they are thought to play an important role in pain signaling. Although the functional properties of Nav1.8 have been relatively well characterized, difficulties with expressing Nav1.9 in established heterologous systems limit our understanding of the gating properties and toxin pharmacology of this particular isoform. This review summarizes our current knowledge of the role of Nav1.8 and Nav1.9 in pain perception and elaborates on the approaches used to identify molecules capable of influencing their function.

Indexed as

AnimalsHumansNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelPainPain PerceptionToxins, BiologicalNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelToxins, Biologicalanimal toxinsNav1.8Nav1.9painvoltage-activated sodium channelvoltage sensor

Identifiers

PMID23012651
PMCPMC3446747

What OpenQuestion holds

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LicenceCC BY
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.