Evidence map›Paper›PMID 24863931›Full record

ArticleThe Journal of general physiology2014

Interactions between permeation and gating in the TMEM16B/anoctamin2 calcium-activated chloride channel.

Giulia Betto, O Lijo Cherian, Simone Pifferi, Valentina Cenedese, Anna Boccaccio, Anna Menini

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
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  12. Article
  13. Article
  14. Article
  15. Epithelial transport inThe Journal of general physiology · 2017
    Review
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  19. Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Giulia BettoNeurobiology Group, International School for Advanced Studies (SISSA), 34136 Trieste, Italy.
O Lijo CherianNeurobiology Group, International School for Advanced Studies (SISSA), 34136 Trieste, Italy.
Simone PifferiNeurobiology Group, International School for Advanced Studies (SISSA), 34136 Trieste, Italy.
Valentina CenedeseNeurobiology Group, International School for Advanced Studies (SISSA), 34136 Trieste, Italy.
Anna BoccaccioIstituto di Biofisica, Consiglio Nazionale delle Ricerche, 16149 Genova, Italy boccaccio@ge.ibf.cnr.it.
Anna MeniniNeurobiology Group, International School for Advanced Studies (SISSA), 34136 Trieste, Italy.
Scuola Internazionale Superiore di Studi Avanzati · ITInstituto Biofisika · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At least two members of the TMEM16/anoctamin family, TMEM16A (also known as anoctamin1) and TMEM16B (also known as anoctamin2), encode Ca(2+)-activated Cl(-) channels (CaCCs), which are found in various cell types and mediate numerous physiological functions. Here, we used whole-cell and excised inside-out patch-clamp to investigate the relationship between anion permeation and gating, two processes typically viewed as independent, in TMEM16B expressed in HEK 293T cells. The permeability ratio sequence determined by substituting Cl(-) with other anions (PX/PCl) was SCN(-) > I(-) > NO3 (-) > Br(-) > Cl(-) > F(-) > gluconate. When external Cl(-) was substituted with other anions, TMEM16B activation and deactivation kinetics at 0.5 µM Ca(2+) were modified according to the sequence of permeability ratios, with anions more permeant than Cl(-) slowing both activation and deactivation and anions less permeant than Cl(-) accelerating them. Moreover, replacement of external Cl(-) with gluconate, or sucrose, shifted the voltage dependence of steady-state activation (G-V relation) to more positive potentials, whereas substitution of extracellular or intracellular Cl(-) with SCN(-) shifted G-V to more negative potentials. Dose-response relationships for Ca(2+) in the presence of different extracellular anions indicated that the apparent affinity for Ca(2+) at +100 mV increased with increasing permeability ratio. The apparent affinity for Ca(2+) in the presence of intracellular SCN(-) also increased compared with that in Cl(-). Our results provide the first evidence that TMEM16B gating is modulated by permeant anions and provide the basis for future studies aimed at identifying the molecular determinants of TMEM16B ion selectivity and gating.

Indexed as

AnimalsAnoctaminsCalciumCell MembraneCell Membrane PermeabilityChloride ChannelsChlorineHEK293 CellsHumansIon Channel GatingMembrane PotentialsMiceStructure-Activity RelationshipANO2 protein, mouseAnoctaminsCalciumChloride ChannelsChlorine

Identifiers

PMID24863931
PMCPMC4035747
OpenAlexW2114000936

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.