Evidence map›Paper›PMID 24835998›Full record

ArticleCell reports2014

Ca2+/calcineurin-dependent inactivation of neuronal L-type Ca2+ channels requires priming by AKAP-anchored protein kinase A.

Philip J Dittmer, Mark L Dell'Acqua, William A Sather

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. αeLife · 2023
    Article
  7. Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023
    Review
  8. The CaNeuropharmacology · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. CaCells · 2020
    Article
  15. Article
  16. Article
  17. βAnnual review of pharmacology and toxicology · 2020
    Review
  18. Synaptic crosstalk conferred by a zone of differentially regulated CaProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  20. Preferential generation of CaThe Journal of biological chemistry · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Philip J DittmerDepartment of Pharmacology, University of Colorado School of Medicine, Mail Stop 8315, 12800 East 19(th) Avenue, Aurora, CO 80045, USA.
Mark L Dell'AcquaDepartment of Pharmacology, University of Colorado School of Medicine, Mail Stop 8315, 12800 East 19(th) Avenue, Aurora, CO 80045, USA.
William A SatherDepartment of Pharmacology, University of Colorado School of Medicine, Mail Stop 8315, 12800 East 19(th) Avenue, Aurora, CO 80045, USA. Electronic address: william.sather@ucdenver.edu.
University of Colorado Denver · US

Funding

POSTGRADUATE TRAINING IN CARDIOVASCULAR RESEARCHT32HL007822 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BUTTRICK, PETER N., LEINWAND, LESLIE ANNE · 1996 to 2023
$6.2M
BEHAVIORAL PHARMACOGENETICS OF DRUG AND ALCOHOL ABUSET32AA007464 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI HOFFMAN, PAULA · 1987 to 2017
$4.8M
Mechanisms of Neuronal Calcineurin-NFAT Synapse-to-Nucleus SignalingR01MH102338 · NIMH · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2014 to 2019
$2.2M
AKAP Regulation of Neuronal L-type Calcium Channel Signaling to the NucleusR01MH080291 · NIMH · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2008 to 2013
$2.2M
Reciprocal Control of Ca2+ Channels by Anchored Protein Kinase A and CalcineurinR01HL088548 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SATHER, WILLIAM A · 2007 to 2010
$1.4M
NHLBI NIH HHS R01 HL088548NHLBI NIH HHS R01-HL088548NHLBI NIH HHS T32 HL007822NIAAA NIH HHS T32 AA007464NIAAA NIH HHS T32-AA007464NIMH NIH HHS R01 MH080291NIMH NIH HHS R01-MH080291NIMH NIH HHS R01 MH102338
6 · The paper itself

Abstract

Within neurons, Ca2+-dependent inactivation (CDI) of voltage-gated L-type Ca2+ channels shapes cytoplasmic Ca2+ signals. CDI is initiated by Ca2+ binding to channel-associated calmodulin and subsequent Ca2+/calmodulin activation of the Ca2+-dependent phosphatase, calcineurin (CaN), which is targeted to L channels by the A-kinase-anchoring protein AKAP79/150. Here, we report that CDI of neuronal L channels was abolished by inhibition of PKA activity or PKA anchoring to AKAP79/150 and that CDI was also suppressed by stimulation of PKA activity. Although CDI was reduced by positive or negative manipulation of PKA, interference with PKA anchoring or activity lowered Ca2+ current density whereas stimulation of PKA activity elevated it. In contrast, inhibition of CaN reduced CDI but had no effect on current density. These results suggest a model wherein PKA-dependent phosphorylation enhances neuronal L current, thereby priming channels to undergo CDI, and Ca2+/calmodulin-activated CaN actuates CDI by reversing PKA-mediated enhancement of channel activity.

Indexed as

Action PotentialsA Kinase Anchor ProteinsAnimalsCalcineurinCalciumCalcium Channels, L-TypeCells, CulturedCyclic AMP-Dependent Protein KinasesNeuronsProtein BindingRatsAkap5 protein, ratA Kinase Anchor ProteinsCalcineurinCalciumCalcium Channels, L-TypeCyclic AMP-Dependent Protein Kinases

Identifiers

PMID24835998
PMCPMC4164350
OpenAlexW2097989259

What OpenQuestion holds

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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.