Evidence map›Paper›PMID 21521762›Full record

ArticleThe Journal of physiology2011

Robust L-type calcium current expression following heterozygous knockout of the Cav1.2 gene in adult mouse heart.

Barbara Rosati, Qinghong Yan, Mi Sun Lee, Shian-Ren Liou, Brian Ingalls, Jason Foell, Timothy J Kamp, David McKinnon

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Selective blockade of CaNature communications · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Transmural gradients in ion channel and auxiliary subunit expression.Progress in biophysics and molecular biology · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. L-type CaWiley interdisciplinary reviews. Membrane transport and signaling · 2014
    Article
  18. Article
  19. Multilayered regulation of cardiac ion channels.Biochimica et biophysica acta · 2013
    Review
  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

8 authors at 4 institutions in 4 countries.

Barbara RosatiDepartment of Physiology and Biophysics, BST Room 124, Level 6, Stony Brook University, Stony Brook, NY 11794-8661, USA. brosati@notes.cc.sunysb.edu
Qinghong Yan
Mi Sun Lee
Shian-Ren Liou
Brian Ingalls
Jason Foell
Timothy J Kamp
David McKinnon
Stony Brook University · USUniversity of Wisconsin–Madison · USInstitute of Neurobiology · BGUniversity of Waterloo · CA

Funding

Support CoreP01HL028958 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI ROSEN, MICHAEL R. · 1985 to 2007
$17.6M
NHLBI NIH HHS HL-28958NHLBI NIH HHS P01 HL028958
6 · The paper itself

Abstract

Mechanisms that contribute to maintaining expression of functional ion channels at relatively constant levels following perturbations of channel biosynthesis are likely to contribute significantly to the stability of electrophysiological systems in some pathological conditions. In order to examine the robustness of L-type calcium current expression, the response to changes in Ca²⁺ channel Cav1.2 gene dosage was studied in adult mice. Using a cardiac-specific inducible Cre recombinase system, Cav1.2 mRNA was reduced to 11 ± 1% of control values in homozygous floxed mice and the mice died rapidly (11.9 ± 3 days) after induction of gene deletion. In these homozygous knockout mice, echocardiographic analysis showed that myocardial contractility was reduced to 14 ± 1% of control values shortly before death. For these mice, no effective compensatory changes in ion channel gene expression were triggered following deletion of both Cav1.2 alleles, despite the dramatic decay in cardiac function. In contrast to the homozygote knockout mice, following knockout of only one Cav1.2 allele, cardiac function remained unchanged, as did survival.Cav1.2mRNAexpression in the left ventricle of heterozygous knockout mice was reduced to 58 ± 3% of control values and there was a 21 ± 2% reduction in Cav1.2 protein expression. There was no significant reduction in L-type Ca²⁺ current density in these mice. The results are consistent with a model of L-type calcium channel biosynthesis in which there are one or more saturated steps, which act to buffer changes in both total Cav1.2 protein and L-type current expression.

Indexed as

Genetic Carrier ScreeningAge FactorsAllelesAnimalsCalcium Channels, L-TypeFemaleGene DosageGene Expression RegulationHumansMaleMiceMice, KnockoutMice, TransgenicMutationMyocytes, CardiacCACNA1C protein, mouseCalcium Channels, L-Type

Identifiers

PMID21521762
PMCPMC3145939
OpenAlexW2166338434

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.