Evidence map›Paper›PMID 19307298›Full record

ArticleThe Journal of physiology2009

Human ClCa1 modulates anionic conduction of calcium-dependent chloride currents.

Martine Hamann, Adele Gibson, Noel Davies, Amanda Jowett, Jean Philippe Walhin, Leanne Partington, Karen Affleck, Derek Trezise, Martin Main

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
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  4. Endogenous ion channels expressed in human embryonic kidney (HEK-293) cells.Pflugers Archiv : European journal of physiology · 2022
    Review
  5. Review
  6. CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A.International journal of molecular sciences · 2021
    Article
  7. Article
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  11. Article
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  14. Review
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  17. Article
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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

9 authors at 2 institutions in 1 country.

Martine HamannLeicester University, Department of Cell Physiology and Pharmacology, Medical Sciences Building, PO Box 138, University Road, Leicester LE1 9HN, UK. mh86@le.ac.uk
Adele Gibson
Noel Davies
Amanda Jowett
Jean Philippe Walhin
Leanne Partington
Karen Affleck
Derek Trezise
Martin Main
GlaxoSmithKline (United Kingdom) · GBUniversity of Leicester · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Proteins of the CLCA gene family including the human ClCa1 (hClCa1) have been suggested to constitute a new family of chloride channels mediating Ca(2+)-dependent Cl- currents. The present study examines the relationship between the hClCa1 protein and Ca(2+)-dependent Cl- currents using heterologous expression of hClCa1 in HEK293 and NCIH522 cell lines and whole cell recordings. By contrast to previous reports claiming the absence of Cl- currents in HEK293 cells, we find that HEK293 and NCIH522 cell lines express constitutive Ca(2+)-dependent Cl- currents and show that hClCa1 increases the amplitude of Ca(2+)-dependent Cl- currents in those cells. We further show that hClCa1 does not modify the permeability sequence but increases the Cl- conductance while decreasing the G(SCN-)/G(Cl-) conductance ratio from approximately 2-3 to approximately 1. We use an Eyring rate theory (two barriers, one site channel) model and show that the effect of hClCa1 on the anionic channel can be simulated by its action on lowering the first and the second energy barriers. We conclude that hClCa1 does not form Ca(2+)-dependent Cl- channels per se or enhance the trafficking/insertion of constitutive channels in the HEK293 and NCIH522 expression systems. Rather, hClCa1 elevates the single channel conductance of endogenous Ca(2+)-dependent Cl- channels by lowering the energy barriers for ion translocation through the pore.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidCalciumCell LineCell Line, TumorCell MembraneChloride ChannelsChloridesElectric StimulationElectrophysiological PhenomenaGene ExpressionGluconatesHumansMembrane PotentialsModels, MolecularNiflumic Acid4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidCalciumChloride ChannelsChloridesCLCA1 protein, humanGluconatesgluconic acidNiflumic AcidthiocyanateThiocyanates

Identifiers

PMID19307298
PMCPMC2691903
OpenAlexW2117955440

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.