Evidence map›Paper›PMID 26837888›Full record

ArticlePflugers Archiv : European journal of physiology2016

The ICl,swell inhibitor DCPIB blocks Kir channels that possess weak affinity for PIP2.

Wu Deng, Rahul Mahajan, Clive M Baumgarten, Diomedes E Logothetis

Open access · greenAbstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. PI(4,5)PAdvances in experimental medicine and biology · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Chloride transport modulators as drug candidates.American journal of physiology. Cell physiology · 2021
    Review
  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

4 authors at 2 institutions in 1 country.

Wu DengDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298, USA.
Rahul MahajanDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298, USA.
Clive M BaumgartenDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298, USA.
Diomedes E LogothetisDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, 23298, USA. delogothetis@vcu.edu.
Virginia Commonwealth University · USBoston University · US

Funding

Structural Determinants of PIP2 RegulationR01HL059949 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Leigh Daniel Plant · 1998 to 2026
$11.6M
Modulation of Kir Channel Function by PhosphorylationR01HL090882 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LOGOTHETIS, DIOMEDES E. · 2009 to 2012
$1.5M
Training In Functional Lipidomics In Cardiovascular & Respiratory DiseasesT32HL094290 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 2009 to 2013
$1.2M
G protein regulation of inwardly rectifying potassium channelsF30HL097582 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MAHAJAN, RAHUL · 2009 to 2012
$126k
NHLBI NIH HHS F30 HL097582NHLBI NIH HHS R01 HL059949NHLBI NIH HHS R01 HL090882NHLBI NIH HHS T32 HL094290
6 · The paper itself

Abstract

Inwardly rectifying K(+) (Kir) channels are important contributors to the resting membrane potential and regulate cellular excitability. The activity of Kir channels depends critically on the phospholipid PIP2. Several modulators of the activity of Kir channels alter the apparent affinity of the channel to PIP2. Channels with high apparent affinity to PIP2 may not respond to a given modulator, but mutations that decrease such affinity can render the channel susceptible to modulation. Here, we identify a known inhibitor of the swelling-activated Cl(-) current, DCPIB, as an effective inhibitor of a number of Kir channels both in native cardiac cells and in heterologous expression systems. We show that the apparent affinity to PIP2 determines whether DCPIB will serve as an efficient blocker of Kir channels. These effects are consistent with a model in which DCPIB competes with PIP2 for a common binding site.

Indexed as

Action PotentialsAnimalsCells, CulturedCell SizeChloride ChannelsCyclopentanesIndansMyocytes, CardiacPhosphatidylinositol 4,5-DiphosphatePotassium Channels, Inwardly RectifyingRabbitsXenopus4-(2-butyl-6,7-dichlor-2-cyclopentyl-indan-1-one-5-yl)oxybutyric acidChloride ChannelsCyclopentanesIndansPhosphatidylinositol 4,5-DiphosphatePotassium Channels, Inwardly RectifyingDCPIBKir channelsPatch clampPIP2Two-electrode voltage clamp

Identifiers

PMID26837888
PMCPMC5317042
OpenAlexW2259280555

What OpenQuestion holds

Textmetadata
LicenceTDM
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.