Evidence map›Paper›PMID 16183882›Full record

ArticleBiophysical journal2005

The block of CFTR by scorpion venom is state-dependent.

Matthew D Fuller, Zhi-Ren Zhang, Guiying Cui, Nael A McCarty

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Tweaking the catalytic efficiency of the CFTR ion channel.The Journal of general physiology · 2023
    Article
  3. Article
  4. Article
  5. Positioning of extracellular loop 1 affects pore gating of the cystic fibrosis transmembrane conductance regulator.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. 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.

Matthew D FullerProgram in Molecular and Systems Pharmacology, Emory University, Atlanta, Georgia 30332-0230, USA.
Zhi-Ren Zhang
Guiying Cui
Nael A McCarty
Georgia Institute of Technology · USEmory University · US

Funding

The Dynamic Nature of the CFTR Channel Pore: Coupling Gating to PermeationR01DK056481 · NIDDK · GEORGIA INSTITUTE OF TECHNOLOGY · PI MCCARTY, NAEL A · 2001 to 2013
$2.4M
The Dynamic Nature of the CFTR Channel Pore: Coupling Gating to PermeationR56DK056481 · NIDDK · EMORY UNIVERSITY · PI MCCARTY, NAEL A · 2009 to 2009
$396k
peptide inhibitor: new probe for chloride channelsR21DK066409 · NIDDK · GEORGIA INSTITUTE OF TECHNOLOGY · PI MCCARTY, NAEL A · 2004 to 2005
$289k
NIDDK NIH HHS DK-066409NIDDK NIH HHS DK-56481NIDDK NIH HHS R01 DK056481NIDDK NIH HHS R21 DK066409NIDDK NIH HHS R56 DK056481
6 · The paper itself

Abstract

Cystic fibrosis transmembrane conductance regulator (CFTR) adenosine triphosphate-dependent chloride channels are expressed in epithelial cells and are associated with a number of genetic disorders, including cystic fibrosis. Venom of the scorpion Leirus quinquestriatus hebraeus reversibly inhibits CFTR when applied to its cytoplasmic surface. To examine the state-dependence of inhibition we recorded wild-type and mutant CFTR channel currents using inside-out membrane patches from Xenopus oocytes. Application of either venom or diphenylamine-2-carboxylate to channels that were either activated (open) or resting (closed) indicate primarily closed state-dependent inhibition of CFTR by venom, whereas diphenylamine-2-carboxylate showed no state-dependence of block. Efficacy of venom-mediated macroscopic current inhibition was inversely related to channel activity. Analysis of single-channel and macropatch data indicated that venom could either inhibit channel opening, if it binds during an interburst closed state or in the absence of cytosolic adenosine triphosphate, or introduce new intraburst closed states, if it binds during an open event. The on-rate of venom binding for intraburst block could be modulated by changing CFTR activity with vanadate or adenylyl-imidodiphosphate, or by introducing the Walker A mutation K1250A. These findings represent the first description of state-dependent inhibition of CFTR and suggest that the active toxin could be used as a tool to study the conformational changes that occur during CFTR gating.

Indexed as

AnimalsCells, CulturedCystic Fibrosis Transmembrane Conductance RegulatorDose-Response Relationship, DrugIon Channel GatingMembrane PotentialsOocytesortho-AminobenzoatesScorpion VenomsXenopus laevisCystic Fibrosis Transmembrane Conductance Regulatorfenamic acidortho-AminobenzoatesScorpion Venoms

Identifiers

PMID16183882
PMCPMC1366962
OpenAlexW2047312923

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.