Evidence map›Paper›PMID 17293861›Full record

ArticleNature neuroscience2007

Alternative splicing controls G protein-dependent inhibition of N-type calcium channels in nociceptors.

Jesica Raingo, Andrew J Castiglioni, Diane Lipscombe

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 167 citations in OpenAlex.

  1. Channels (Austin, Tex.) · 2026
    Article
  2. Article
  3. Nociceptor-enriched CAPS1 isoform couples to CabioRxiv : the preprint server for biology · 2026
    Article
  4. bioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Targeted ubiquitination of sensory neuron calcium channels reduces the development of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Heat But Not Mechanical Hypersensitivity Depends on Voltage-Gated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jesica RaingoDepartment of Neuroscience, Brown University, Sidney E. Frank Hall for Life Sciences, 185 Meeting Street, Providence, Rhode Island 02912, USA.
Andrew J Castiglioni
Diane Lipscombe
Brown University · US

Funding

Voltage-Gated Calcium Channels in Nociceptors and MechanoreceptorsR01NS055251 · NINDS · BROWN UNIVERSITY · PI LIPSCOMBE, DIANE · 2006 to 2025
$9.1M
TRAINING IN MOLECULAR &CELL BIOLOGY &BIOCHEMISTRYT32GM007601 · NIGMS · BROWN UNIVERSITY · PI MOWRY, KIMBERLY L. · 1985 to 2019
$6.4M
NEURONAL CALCIUM CHANNELS--REGULATION AND FUNCTIONR01NS029967 · NINDS · BROWN UNIVERSITY · PI LIPSCOMBE, DIANE · 1997 to 2009
$3.0M
NEURONAL CALIUM CHANNELS--REGULATION AND FUNCTIONR29NS029967 · NINDS · BROWN UNIVERSITY · PI LIPSCOMBE, DIANE · 1992 to 1996
–
NIGMS NIH HHS T32 GM007601NINDS NIH HHS NS29967NINDS NIH HHS NS55251NINDS NIH HHS R01 NS029967NINDS NIH HHS R01 NS055251
6 · The paper itself

Abstract

Neurotransmitter release from mammalian sensory neurons is controlled by Ca(V)2.2 N-type calcium channels. N-type channels are a major target of neurotransmitters and drugs that inhibit calcium entry, transmitter release and nociception through their specific G protein-coupled receptors. G protein-coupled receptor inhibition of these channels is typically voltage-dependent and mediated by Gbetagamma, whereas N-type channels in sensory neurons are sensitive to a second G protein-coupled receptor pathway that inhibits the channel independent of voltage. Here we show that preferential inclusion in nociceptors of exon 37a in rat Cacna1b (encoding Ca(V)2.2) creates, de novo, a C-terminal module that mediates voltage-independent inhibition. This inhibitory pathway requires tyrosine kinase activation but not Gbetagamma. A tyrosine encoded within exon 37a constitutes a critical part of a molecular switch controlling N-type current density and G protein-mediated voltage-independent inhibition. Our data define the molecular origins of voltage-independent inhibition of N-type channels in the pain pathway.

Indexed as

Alternative SplicingAnalgesics, OpioidAnimalsBaclofenCalciumCalcium Channels, N-TypeCell LineElectric StimulationEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Enzyme InhibitorsExonsGABA AgonistsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)HumansMembrane PotentialsAnalgesics, OpioidBaclofenCacna1b protein, ratCalciumCalcium Channels, N-TypeEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Enzyme InhibitorsGABA AgonistsGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)

Identifiers

PMID17293861
PMCPMC3027493
OpenAlexW1982797011

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.