Evidence map›Paper›PMID 18945938›Full record

ArticleAmerican journal of physiology. Cell physiology2008

Expression, localization, and functional properties of Bestrophin 3 channel isolated from mouse heart.

Kate E O'Driscoll, William J Hatton, Heather R Burkin, Normand Leblanc, Fiona C Britton

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. CaActa physiologica (Oxford, England) · 2026
    Review
  3. Review
  4. Isogenic iPSC-derivedFrontiers in neuroscience · 2025
    Article
  5. Article
  6. Review
  7. Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020
    Review
  8. Human cytomegalovirus US21 protein is a viroporin that modulates calcium homeostasis and protects cells against apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014
    Review
  14. Article
  15. Review
  16. Phenomics of cardiac chloride channels.Comprehensive Physiology · 2013
    Review
  17. Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Kate E O'DriscollDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, USA.
William J Hatton
Heather R Burkin
Normand Leblanc
Fiona C Britton
University of Nevada, Reno · US

Funding

Signal transduction pathways regulated by cell volumeP20RR015581 · NCRR · UNIVERSITY OF NEVADA RENO · PI VALENCIK, MARIA LYNN · 2000 to 2009
$19.5M
Bestrophin Channel Function in HeartR01HL091238 · NHLBI · UNIVERSITY OF NEVADA RENO · PI BRITTON, FIONA CATHERINE · 2008 to 2012
$2.0M
Properties of Clca Channels in Vascular MyocytesR01HL075477 · NHLBI · UNIVERSITY OF NEVADA RENO · PI LEBLANC, NORMAND · 2005 to 2009
$1.7M
NCRR NIH HHS P 20RR 15581NHLBI NIH HHS R01 HL-075477-01NHLBI NIH HHS R01 HL091238NHLBI NIH HHS R01 HL-091238-01A1
6 · The paper itself

Abstract

Bestrophins are a novel family of proteins that encode calcium-activated chloride channels. In this study we establish that Bestrophin transcripts are expressed in the mouse and human heart. Native mBest3 protein expression and localization in heart was demonstrated by using a specific polyclonal mBest3 antibody. Immunostaining of isolated cardiac myocytes indicates that mBest3 is present at the membrane. Using the patch-clamp technique, we characterized the biophysical and pharmacological properties of mBest3 cloned from heart. Whole cell chloride currents were evoked in both HEK293 and COS-7 cells expressing mBest3 by elevation of intracellular calcium. mBest3 currents displayed a K(D) for Ca(2+) of approximately 175 nM. The calcium-activated chloride current was found to be time and voltage independent and displayed slight outward rectification. The anion permeability sequence of the channel was SCN(-)>I(-)>Cl(-), and the current was inhibited by niflumic acid and DIDS in the micromolar range. In addition, we generated a site-specific mutation (F80L) in the putative pore region of mBest3 that significantly altered the ion conduction and pharmacology of this channel. Our functional and mutational studies examining the biophysical properties of mBest3 indicate that it functions as a pore-forming chloride channel that is activated by physiological levels of calcium. This study reports novel findings regarding the molecular expression, tissue localization, and functional properties of mBest3 cloned from heart.

Indexed as

Amino Acid SequenceAnimalsBestrophinsBlotting, WesternChloride ChannelsHeartHumansMiceMice, Inbred BALB CMicroscopy, ConfocalMolecular Sequence DataMuscle ProteinsMutagenesis, Site-DirectedPatch-Clamp TechniquesReverse Transcriptase Polymerase Chain ReactionSequence Homology, Amino AcidBEST3 protein, humanBestrophinsChloride ChannelsMuscle Proteins

Identifiers

PMID18945938
PMCPMC2603566
OpenAlexW2103302777

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.