Evidence map›Paper›PMID 14724744›Full record

ArticleThe Journal of membrane biology2003

Characterization of a functionally expressed stretch-activated BKca channel cloned from chick ventricular myocytes.

Q Y Tang, Z Qi, K Naruse, M Sokabe

Abstract readComparative StudyEvaluation Study
PubMed Publisher
In one paragraph

Article in The Journal of membrane biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Mechanotransduction-Driven Modulation ofInternational journal of molecular sciences · 2025
    Article
  2. The mechanism of CaThe Journal of biological chemistry · 2025
    Article
  3. Article
  4. Inhibition of BKCell death discovery · 2022
    Article
  5. Review
  6. BKAntioxidants (Basel, Switzerland) · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. BK channels regulate sinoatrial node firing rate and cardiac pacing in vivo.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  12. Article
  13. Mechanobiology in cardiac physiology and diseases.Journal of cellular and molecular medicine · 2013
    Review
  14. Review
  15. Article
  16. Article
  17. Mechanosensitive ion channels and the peptide inhibitor GsMTx-4: history, properties, mechanisms and pharmacology.Toxicon : official journal of the International Society on Toxinology · 2007
    Review
  18. Twenty odd years of stretch-sensitive channels.Pflugers Archiv : European journal of physiology · 2006
    Review
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

4 authors at 1 institution in 1 country.

Q Y TangDepartment of Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Z Qi
K Naruse
M Sokabe
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have characterized electrophysiological and pharmacological properties of a stretch-activated BKca channel (SAKcaC) that was cloned from cultured chick ventricular myocytes (CCVM) and expressed in chinese hamster ovary cells (CHO) using the patch-clamp technique. Our results indicate that the cloned SAKcaC keeps most of the key properties of the native SAKcaC in CCVM, such as conductance, ion selectivity, pressure-, voltage- and Ca(2+)-dependencies. However, there was a slight difference between these channels in the effects of channel blockers, charybdotoxin (CTX) and gadolinium (Gd(3+)). The native SAKcaC was blocked in an all-or-none fashion characterized as the slow blockade, whereas the conductance of the cloned SAKcaC was gradually decreased with the blockers' concentration, without noticeable blocking noise. As the involvement of some auxiliary components was suspected in this difference, we cloned a BK beta-subunit from CCVM and coexpressed it with the cloned SAKcaC in CHO cells to examine its effects on the SAKcaC. Although the pharmacological properties of the cloned SAKcaC turned out to be very similar to the native one by the coexpression, it also significantly altered the key characteristics of SAKcaC, such as voltage- and Ca(2+)-dependencies. Therefore we concluded that the native SAKca in CCVM does not interact with the corresponding endogenous beta-subunit. The difference in pharmacological properties between the expressed SAKcaC in CHO and the native one in CCVM suggests that the native SAKca in CCVM is modulated by unknown auxiliary components.

Indexed as

AnimalsCalciumChick EmbryoCHO CellsCloning, MolecularConotoxinsCricetinaeCricetulusDose-Response Relationship, DrugGadoliniumIon Channel GatingLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane PotentialsMyocytes, CardiacPotassium ChannelsPressureCalciumConotoxinsGadoliniumKcnma1 protein, ratLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsPotassium ChannelsRecombinant ProteinsTetraethylammonium

Identifiers

PMID14724744
OpenAlexW1974683581

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.