Evidence map›Paper›PMID 26024338›Full record

ArticleBiochemistry2015

The Fifth Transmembrane Segment of Cystic Fibrosis Transmembrane Conductance Regulator Contributes to Its Anion Permeation Pathway.

Jingyao Zhang, Tzyh-Chang Hwang

Abstract read
In one paragraph

Article in Biochemistry, 2015. 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
3.8field-weighted citation impact, top 6% 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, 20 citations in OpenAlex.

  1. CFTR Modulators: From Mechanism to Targeted Therapeutics.Handbook of experimental pharmacology · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Structural mechanisms of CFTR function and dysfunction.The Journal of general physiology · 2018
    Review
  7. Article
  8. Article
  9. Architecture and functional properties of the CFTR channel pore.Cellular and molecular life sciences : CMLS · 2017
    Review
  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

2 authors at 1 institution in 1 country.

Jingyao Zhang†Department of Biological Engineering, University of Missouri-Columbia, 254 Agricultural Engineering, Columbia, Missouri 65211, United States.
Tzyh-Chang Hwang†Department of Biological Engineering, University of Missouri-Columbia, 254 Agricultural Engineering, Columbia, Missouri 65211, United States.
University of Missouri · US

Funding

MOLECULAR PATHOPHYSIOLOGY OF CYSTIC FIBROSISR01DK055835 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI HWANG, TZYH-CHANG · 1999 to 2022
$6.1M
NIDDK NIH HHS R01 DK055835NIDDK NIH HHS R01DK55835
6 · The paper itself

Abstract

Previous studies have identified several transmembrane segments (TMs), including TM1, TM3, TM6, TM9, TM11, and TM12, as pore-lining segments in cystic fibrosis transmembrane conductance regulator (CFTR), but the role of TM5 in pore construction remains controversial. In this study, we employed substituted cysteine accessibility methodology (SCAM) to screen the entire TM5 defined by the original topology model and its cytoplasmic extension in a Cysless background. We found six positions (A299, R303, N306, S307, F310, and F311) where engineered cysteines react to intracellular 2-sulfonatoethyl methanethiosulfonate (MTSES⁻). Quantification of the modification rate of engineered cysteines in the presence or absence of ATP suggests that these six residues are accessible in both the open and closed states. Whole-cell experiments with external MTSES⁻ identified only two positive positions (L323 and A326), resulting in a segment containing 11 consecutive amino acids, where substituted cysteines respond to neither internal nor external MTSES⁻, a unique feature not seen previously in CFTR's pore-lining segments. The observation that these positions are inaccessible to channel-permeant thiol-specific reagent [Au(CN)₂]⁻ suggests that this segment of TM5 between F311 and L323 is concealed from the pore by other TMs and/or lipid bilayers. In addition, our data support the idea that the positively charged arginine at position 303 poses a pure electrostatic action in determining the single-channel current amplitude of CFTR and the effect of an open-channel blocker glibencalmide. Collectively, we conclude that the cytoplasmic portion of CFTR's TM5 lines the pore. Our functional data are remarkably consistent with predicted structural arrangements of TM5 in some homology models of CFTR.

Indexed as

Cell Membrane PermeabilityModels, MolecularAmino Acid SubstitutionAnimalsCHO CellsCricetulusCysteineCystic Fibrosis Transmembrane Conductance RegulatorHumansMesylatesMutant ProteinsPatch-Clamp TechniquesPeptide FragmentsProtein ConformationProtein EngineeringProtein Structure, Tertiary(2-sulfonatoethyl)methanethiosulfonateCFTR protein, humanCysteineCystic Fibrosis Transmembrane Conductance RegulatorMesylatesMutant ProteinsPeptide FragmentsRecombinant ProteinsSulfhydryl Reagents

Identifiers

PMID26024338
PMCPMC6510985
OpenAlexW2412457087

What OpenQuestion holds

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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.