Evidence map›Paper›PMID 12719232›Full record

ArticleBiophysical journal2003

Distinctive modulatory effects of five human auxiliary beta2 subunit splice variants on L-type calcium channel gating.

Shoji X Takahashi, Scott Mittman, Henry M Colecraft

Open access · bronzeAbstract readComparative StudyEvaluation StudyValidation Study
In one paragraph

Article in Biophysical journal, 2003. 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
3.0field-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

70 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Acute phosphatidylinositol 4,5 bisphosphate depletion destabilizes sarcolemmal expression of cardiac L-type CaProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Electrically regulated cell-based intervention for viral infections.Bioengineering & translational medicine · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. β-Adrenergic control of sarcolemmal CaProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. The βFrontiers in cardiovascular medicine · 2021
    Article
  13. Review
  14. Review
  15. Review
  16. Diabetes · 2019
    Article
  17. Article
  18. Review
  19. Article
  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

3 authors at 2 institutions in 1 country.

Shoji X TakahashiCalcium Signals Laboratory, Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Scott Mittman
Henry M Colecraft
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Molecular Determinants of L-type Calcium Channel GatingR01HL069911 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI COLECRAFT, HENRY M. · 2002 to 2011
$3.3M
NHLBI NIH HHS R01 HL069911NHLBI NIH HHS R01 HL-69911
6 · The paper itself

Abstract

Sequence analysis of the human genome permitted cloning of five Ca(2+)-channel beta(2) splice variants (beta(2a)-beta(2e)) that differed only in their proximal amino-termini. The functional consequences of such beta(2)-subunit diversity were explored in recombinant L-type channels reconstituted in HEK 293 cells. Beta(2a) and beta(2e) targeted autonomously to the plasma membrane, whereas beta(2b)-beta(2d) localized to the cytosol when expressed in HEK 293 cells. The pattern of modulation of L-type channel voltage-dependent inactivation gating correlated with the subcellular localization of the component beta(2) variant-membrane-bound beta(2a) and beta(2e) subunits conferred slow(er) channel inactivation kinetics and displayed a smaller fraction of channels recovering from inactivation with fast kinetics, compared to beta(2b)-beta(2d) channels. The varying effects of beta(2) subunits on inactivation gating were accounted for by a quantitative model in which L-type channels reversibly distributed between fast and slow forms of voltage-dependent inactivation-membrane-bound beta(2) subunits substantially decreased the steady-state fraction of fast inactivating channels. Finally, the beta(2) variants also had distinctive effects on L-type channel steady-state activation gating, as revealed by differences in the waveforms of tail-activation (G-V) curves, and conferred differing degrees of prepulse facilitation to the channel. Our results predict important physiological consequences arising from subtle changes in Ca(2+)-channel beta(2)-subunit structure due to alternative splicing and emphasize the utility of splice variants in probing structure-function mechanisms.

Indexed as

MutationSequence AlignmentAdaptation, PhysiologicalBrainCalcium Channels, L-TypeCells, CulturedCloning, MolecularGenetic VariationHomeostasisHumansIon Channel GatingKidneyKineticsMembrane PotentialsMyocardiumProtein SubunitsCACNB2 protein, humanCalcium Channels, L-TypeProtein SubunitsRecombinant Proteins

Identifiers

PMID12719232
PMCPMC1302863
OpenAlexW2009291123

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.