Evidence map›Paper›PMID 24120865›Full record

ArticleCell reports2013

Continuously tunable Ca(2+) regulation of RNA-edited CaV1.3 channels.

Hojjat Bazzazi, Manu Ben Johny, Paul J Adams, Tuck Wah Soong, David T Yue

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.4field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025
    Review
  4. Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023
    Review
  5. Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023
    Article
  6. Review
  7. Loss of CaProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Tuberous Sclerosis Complex (TSC) Inactivation Increases Neuronal Network Activity by Enhancing CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. CaThe Journal of biological chemistry · 2020
    Article
  12. Review
  13. Article
  14. Conservation of cardiac L-type CaJournal of molecular and cellular cardiology · 2018
    Article
  15. CaBP1 regulates CaMolecular and cellular neurosciences · 2018
    Article
  16. Bilobal architecture is a requirement for calmodulin signaling to CaProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Article
  18. Article
  19. 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 3 institutions in 2 countries.

Hojjat BazzaziCalcium Signals Laboratory, Departments of Biomedical Engineering and Neuroscience, The Johns Hopkins University School of Medicine, Ross Building, Room 713, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Manu Ben Johny
Paul J Adams
Tuck Wah Soong
David T Yue
Johns Hopkins University · USJohns Hopkins Medicine · USNational University of Singapore · SG

Funding

Ca Regulation of Ca ChannelsR01MH065531 · NIMH · JOHNS HOPKINS UNIVERSITY · PI JOHNY, MANU BEN · 2002 to 2016
$5.7M
Calmodulin/Ca Channel Physiology in HeartR37HL076795 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI YUE, DAVID T · 2004 to 2013
$4.1M
NHLBI NIH HHS R37 HL076795NIMH NIH HHS R01 MH065531
6 · The paper itself

Abstract

CaV1.3 ion channels are dominant Ca(2+) portals into pacemaking neurons, residing at the epicenter of brain rhythmicity and neurodegeneration. Negative Ca(2+) feedback regulation of CaV1.3 channels (CDI) is therefore critical for Ca(2+) homeostasis. Intriguingly, nearly half the CaV1.3 transcripts in the brain are RNA edited to reduce CDI and influence oscillatory activity. It is then mechanistically remarkable that this editing occurs precisely within an IQ domain, whose interaction with Ca(2+)-bound calmodulin (Ca(2+)/CaM) is believed to induce CDI. Here, we sought the mechanism underlying the altered CDI of edited channels. Unexpectedly, editing failed to attenuate Ca(2+)/CaM binding. Instead, editing weakened the prebinding of Ca(2+)-free CaM (apoCaM) to channels, which proves essential for CDI. Thus, editing might render CDI continuously tunable by fluctuations in ambient CaM, a prominent effect we substantiate in substantia nigral neurons. This adjustability of Ca(2+) regulation by CaM now looms as a key element of CNS Ca(2+) homeostasis.

Indexed as

Amino Acid SequenceAnimalsCalciumCalcium Channels, L-TypeCalmodulinCells, CulturedHEK293 CellsHumansMiceMice, Inbred C57BLMolecular Sequence DataNeuronsPatch-Clamp TechniquesProtein BindingProtein Structure, TertiaryRNACACNA1D protein, humanCalciumCalcium Channels, L-TypeCalmodulinRNA

Identifiers

PMID24120865
PMCPMC4349392
OpenAlexW1972880122

What OpenQuestion holds

Textmetadata
LicenceTDM
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.