Evidence map›Paper›PMID 19679661›Full record

ArticleThe Journal of biological chemistry2009

Loss of TMEM16A causes a defect in epithelial Ca2+-dependent chloride transport.

Jiraporn Ousingsawat, Joana R Martins, Rainer Schreiber, Jason R Rock, Brian D Harfe, Karl Kunzelmann

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Restoring chloride efflux in cystic fibrosis with TMEM16a antisense oligonucleotides.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. CaPhysiological reviews · 2024
    Review
  10. Article
  11. Article
  12. Intestinal secretory mechanisms and diarrhea.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Review
  13. EnterotoxigenicPathogens (Basel, Switzerland) · 2022
    Review
  14. Pharmaceutical biology · 2021
    Article
  15. Is white the right light for the clinical electrooculogram?Documenta ophthalmologica. Advances in ophthalmology · 2021
    Article
  16. Review
  17. The diverse roles of TMEM16A CaJournal of advanced research · 2021
    Review
  18. Review
  19. An outer-pore gate modulates the pharmacology of the TMEM16A channel.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Article

68 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Jiraporn OusingsawatInstitut für Physiologie, Universität Regensburg, Universitätsstrasse 31, D-93053 Regensburg, Germany.
Joana R Martins
Rainer Schreiber
Jason R Rock
Brian D Harfe
Karl Kunzelmann
University of Regensburg · DEUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular identification of the Ca(2+)-dependent chloride channel TMEM16A (ANO1) provided a fundamental step in understanding Ca(2+)-dependent Cl(-) secretion in epithelia. TMEM16A is an intrinsic constituent of Ca(2+)-dependent Cl(-) channels in cultured epithelia and may control salivary output, but its physiological role in native epithelial tissues remains largely obscure. Here, we demonstrate that Cl(-) secretion in native epithelia activated by Ca(2+)-dependent agonists is missing in mice lacking expression of TMEM16A. Ca(2+)-dependent Cl(-) transport was missing or largely reduced in isolated tracheal and colonic epithelia, as well as hepatocytes and acinar cells from pancreatic and submandibular glands of TMEM16A(-/-) animals. Measurement of particle transport on the surface of tracheas ex vivo indicated largely reduced mucociliary clearance in TMEM16A(-/-) mice. These results clearly demonstrate the broad physiological role of TMEM16A(-/-) for Ca(2+)-dependent Cl(-) secretion and provide the basis for novel treatments in cystic fibrosis, infectious diarrhea, and Sjöegren syndrome.

Indexed as

AnimalsAnoctamin-1CalciumChloride ChannelsChloridesColonCyclic AMPElectrolytesEpithelial CellsHepatocytesIon TransportMiceMice, KnockoutTracheaANO1 protein, mouseAnoctamin-1CalciumChloride ChannelsChloridesCyclic AMPElectrolytes

Identifiers

PMID19679661
PMCPMC2781414
OpenAlexW1976022507

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.