Evidence map›Paper›PMID 28875346›Full record

ArticlePflugers Archiv : European journal of physiology2018

CFTR supports cell death through ROS-dependent activation of TMEM16F (anoctamin 6).

Filipa Simões, Jiraporn Ousingsawat, Podchanart Wanitchakool, Ana Fonseca, Inês Cabrita, Roberta Benedetto, Rainer Schreiber, Karl Kunzelmann

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Ivacaftor attenuates gentamicin-induced ototoxicity through the CFTR-Nrf2-HO1/NQO1 pathway.Redox report : communications in free radical research · 2024
    Article
  6. TMEM16 proteins: CaInternational journal of molecular medicine · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. CaInternational journal of molecular sciences · 2022
    Article
  14. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Ferroptosis and kidney diseases.International urology and nephrology · 2020
    Review
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

8 authors at 1 institution in 1 country.

Filipa SimõesInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Jiraporn OusingsawatInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Podchanart WanitchakoolInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Ana FonsecaInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Inês CabritaInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Roberta BenedettoInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Rainer SchreiberInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany.
Karl KunzelmannInstitut für Physiologie, Universität Regensburg, Universitätsstraße 31, 93053, Regensburg, Germany. karl.kunzelmann@ur.de.
University of Regensburg · DE

Funding

Cystic Fibrosis Trust SRC003 INOVCFDeutsche Forschungsgemeinschaft KU756/12-1Deutsche Forschungsgemeinschaft SFB699ADeutsche Forschungsgemeinschaft SFB699A12
6 · The paper itself

Abstract

Cystic fibrosis transmembrane conductance regulator (CFTR) is the essential chloride and bicarbonate channel in the apical membrane of epithelial cells. CFTR was also proposed earlier to conduct glutathione (GSH) out of airway epithelial cells to be enriched in the apical airway surface liquid to neutralize reactive oxygen species (ROS). Although earlier studies suggested that release of GSH by wild type (wt) CFTR may lead to an increase in cytosolic ROS, we did not detect different ROS levels in cells expressing wt-CFTR and mutant F508del-CFTR, independent of CFTR-activation or exposure to the ROS donor tert-butyl hydroperoxide. The Ca

Indexed as

ApoptosisAnimalsAnoctaminsCystic Fibrosis Transmembrane Conductance RegulatorHEK293 CellsHeLa CellsHumansMicePhospholipid Transfer ProteinsReactive Oxygen SpeciesXenopusANO6 protein, mouseAnoctaminsCystic Fibrosis Transmembrane Conductance RegulatorPhospholipid Transfer ProteinsReactive Oxygen SpeciesAnoctamin 6ApoptosisCFTRCystic fibrosisFerroptosisNecroptosisRegulated cell deathTMEM16F

Identifiers

PMID28875346
OpenAlexW2753387893

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.