Evidence map›Paper›PMID 22223119›Full record

ReviewBiochimica et biophysica acta2012

Ca2+-dependent modulation of voltage-gated Ca2+ channels.

Carl Christel, Amy Lee

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 108 citations in OpenAlex.

  1. The NaThe Journal of veterinary medical science · 2026
    Review
  2. Article
  3. Presynaptic CabioRxiv : the preprint server for biology · 2026
    Article
  4. L-Type Voltage-Gated CaBiochemistry · 2025
    Article
  5. Article
  6. Reduction of the CaFrontiers in cellular neuroscience · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Calmodulin promotes a CaFEBS letters · 2022
    Article
  14. Article
  15. L-Type CaBiomolecules · 2021
    Review
  16. CaCells · 2020
    Article
  17. Review
  18. Rare CACNA1A mutations leading to congenital ataxia.Pflugers Archiv : European journal of physiology · 2020
    Review
  19. Review
  20. Article

10 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

2 authors at 1 institution in 1 country.

Carl ChristelDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, USA.
Amy Lee
University of Iowa · US

Funding

Regulation of auditory calcium channelsR01DC009433 · NIDCD · UNIVERSITY OF IOWA · PI LEE, AMY · 2009 to 2018
$3.6M
Modulation of Cav 1.3 L-type Ca2+ channels by PDZ-protein interactionsR01HL087120 · NHLBI · UNIVERSITY OF IOWA · PI LEE, AMY · 2009 to 2012
$1.4M
Regulation of auditory calcium channelsR55DC009433 · NIDCD · EMORY UNIVERSITY · PI LEE, AMY · 2008 to 2008
$100k
NHLBI NIH HHS HL087120NHLBI NIH HHS R01 HL087120NIDCD NIH HHS DC009433NIDCD NIH HHS R01 DC009433NIDCD NIH HHS R55 DC009433PHS HHS T32007121
6 · The paper itself

Abstract

backgroundVoltage-gated (Cav) Ca2+ channels are multi-subunit complexes that play diverse roles in a wide variety of tissues. A fundamental mechanism controlling Cav channel function involves the Ca2+ ions that permeate the channel pore. Ca2+ influx through Cav channels mediates feedback regulation to the channel that is both negative (Ca2+-dependent inactivation, CDI) and positive (Ca2+-dependent facilitation, CDF). SCOPE OF REVIEW: This review highlights general mechanisms of CDI and CDF with an emphasis on how these processes have been studied electrophysiologically in native and heterologous expression systems. MAJOR

conclusionsElectrophysiological analyses have led to detailed insights into the mechanisms and prevalence of CDI and CDF as Cav channel regulatory mechanisms. All Cav channel family members undergo some form of Ca2+-dependent feedback that relies on CaM or a related Ca2+ binding protein. Tremendous progress has been made in characterizing the role of CaM in CDI and CDF. Yet, what contributes to the heterogeneity of CDI/CDF in various cell-types and how Ca2+-dependent regulation of Cav channels controls Ca2+ signaling remain largely unexplored. GENERAL SIGNIFICANCE: Ca2+ influx through Cav channels regulates diverse physiological events including excitation-contraction coupling in muscle, neurotransmitter and hormone release, and Ca2+-dependent gene transcription. Therefore, the mechanisms that regulate channels, such as CDI and CDF, can have a large impact on the signaling potential of excitable cells in various physiological contexts. This article is part of a Special Issue entitled Biochemical, biophysical and genetic approaches to intracellular calcium signaling.

Indexed as

Calcium SignalingAnimalsCalciumCalcium-Binding ProteinsCalcium ChannelsFeedback, PhysiologicalHumansMembrane PotentialsNeuronsOrgan SpecificityProtein IsoformsProtein SubunitsCalciumCalcium-Binding ProteinsCalcium ChannelsProtein IsoformsProtein Subunits

Identifiers

PMID22223119
PMCPMC3345169
OpenAlexW2124030990

What OpenQuestion holds

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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.