Evidence map›Paper›PMID 28130847›Full record

ArticleThe Journal of physiology2017

Calmodulin and ATP support activity of the Cav1.2 channel through dynamic interactions with the channel.

Etsuko Minobe, Masayuki X Mori, Masaki Kameyama

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023
    Review
  2. Properties of Calmodulin Binding to NaNeurochemical research · 2021
    Article
  3. 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

3 authors at 2 institutions in 1 country.

Etsuko MinobeDepartment of Physiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, 890-8544, Japan.ORCID 0000-0003-1351-0440
Masayuki X MoriLaboratory of Molecular Biology, Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University, Kyoto, 615-8510, Japan.
Masaki KameyamaDepartment of Physiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, 890-8544, Japan.
Kagoshima University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsCav1.2 channels maintain activity through interactions with calmodulin (CaM). In this study, activities of the Cav1.2 channel (α1C) and of mutant-derivatives, C-terminal deleted (α1CΔ) and α1CΔ linked with CaM (α1CΔCaM), were compared in the inside-out mode. α1CΔ with CaM, but not without CaM, and α1CΔCaM were active, suggesting that CaM induced channel activity through a dynamic interaction with the channel, even without the distal C-tail. ATP induced α1C activity with CaM and enhanced activity of the mutant channels. Okadaic acid mimicked the effect of ATP on the wildtype but not mutant channels. These results supported the hypothesis that CaM and ATP maintain activity of Cav1.2 channels through their dynamic interactions. ATP effects involve mechanisms both related and unrelated to channel phosphorylation. CaM-linked channels are useful tools for investigating Cav1.2 channels in the inside-out mode; the fast run-down is prevented by only ATP and the slow run-down is nearly absent. ABSTRACT: Calmodulin (CaM) plays a critical role in regulation of Cav1.2 Ca

Indexed as

Adenosine TriphosphateAnimalsCalcium Channels, L-TypeCalmodulinHEK293 CellsHumansProtein BindingRabbitsRatsAdenosine TriphosphateCalcium Channels, L-TypeCalmodulinL-type calcium channel alpha(1C)ATPcalcium channelcalmodulin

Identifiers

PMID28130847
PMCPMC5390892
OpenAlexW2582148964

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.