Evidence map›Paper›PMID 14602827›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

A mechanism for the direct regulation of T-type calcium channels by Ca2+/calmodulin-dependent kinase II.

Philip J Welsby, Hongge Wang, Joshua T Wolfe, Roger J Colbran, Michael L Johnson, Paula Q Barrett

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

69 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025
    Review
  3. Article
  4. A non-conducting role of the CabioRxiv : the preprint server for biology · 2024
    Article
  5. The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024
    Review
  6. Article
  7. CaMKII and CaCell biology and toxicology · 2023
    Article
  8. Review
  9. Review
  10. Effects of progesterone on T-type-CaNeural regeneration research · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020
    Review
  17. Genetic T-type calcium channelopathies.Journal of medical genetics · 2020
    Review
  18. Article
  19. Article
  20. Article

9 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

6 authors at 2 institutions in 1 country.

Philip J WelsbyDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, USA.
Hongge Wang
Joshua T Wolfe
Roger J Colbran
Michael L Johnson
Paula Q Barrett
University of Virginia · USVanderbilt University · US

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
NHLBI NIH HHS T32 HL007572PHS HHS R01 36977
6 · The paper itself

Abstract

Low-voltage-activated (LVA) Ca2+ channels are widely distributed throughout the CNS and are important determinants of neuronal excitability, initiating dendritic and somatic Ca2+ spikes that trigger and shape the pattern of action potential firing. Here, we define a molecular mechanism underlying the dynamic regulation of alpha1H channels (Cav3.2), by Ca2+/CaM-dependent protein kinase II (CaMKII). We show that channel regulation is selective for the LVA alpha1H Ca2+ channel subtype, depends on determinants in the alpha1H II-III intracellular loop, and requires the phosphorylation of a serine residue absent from unregulated alpha1G (Cav3.1) channels. These studies identify the alpha1H channel as a new substrate for CaMKII and provide the first molecular mechanism for the direct regulation of T-type Ca2+ channels by a protein kinase. Our data suggest a novel mechanism for modulating the integrative properties of neurons.

Indexed as

Binding SitesCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, T-TypeCell LineGene Transfer TechniquesHumansIon Channel GatingKidneyMutagenesis, Site-DirectedPatch-Clamp TechniquesPhosphorylationProtein Structure, TertiaryRecombinant Fusion ProteinsCACNA1G protein, humanCACNA1H protein, humanCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, T-TypeRecombinant Fusion Proteins

Identifiers

PMID14602827
PMCPMC6740846
OpenAlexW1484974990

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.