Evidence map›Paper›PMID 22116367›Full record

ReviewCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011

The role of pendrin in the development of the murine inner ear.

Philine Wangemann

Abstract readReview
In one paragraph

Review in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Inhibitors of pendrin anion exchange identified in a small molecule screen increase airway surface liquid volume in cystic fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  10. The multiple roles of pendrin in the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015
    Review
  11. Article
  12. Article
  13. Review
  14. Anion translocation through an Slc26 transporter mediates lumen expansion during tubulogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. World journal of otorhinolaryngology · 2013
    Article
  16. Article
  17. Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. SLC26A4 genotypes and phenotypes associated with enlargement of the vestibular aqueduct.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011
    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

1 author.

Philine WangemannAnatomy & Physiology Department, Kansas State University, Manhattan, Kansas 66506, USA. wange@vet.ksu.edu

Funding

CYTOSOLIC REGULATION OF INNER EAR ION TRANSPORTR01DC001098 · NIDCD · KANSAS STATE UNIVERSITY · PI WANGEMANN, A. PHILINE · 1997 to 2007
$2.1M
NIDCD NIH HHS R01 DC001098
6 · The paper itself

Abstract

Enlargement of the vestibular aqueduct (EVA) is a common inner ear malformation found in children with sensorineural hearing loss that is frequently associated with loss-of-function or hypo-function mutations of SLC26A4. SLC26A4 codes for pendrin, which is a protein that is expressed in apical membranes of selected epithelia and functions as an anion exchanger. The comparatively high prevalence of EVA provides a strong imperative to develop rational interventions that delay, ameliorate or prevent hearing loss associated with this phenotype. The development of rational interventions requires a fundamental understanding of the role that pendrin plays in the normal development of hearing, as well as a detailed understanding of the pathobiologic mechanisms that, in the absence of fully functional pendrin, lead to an unstable hearing phenotype, with fluctuating or progressive loss of hearing. This review summarizes studies in mouse models that have focused on delineating the role of pendrin in the physiology of the inner ear and the pathobiology that leads to hearing loss.

Indexed as

AnimalsAnionsAnion Transport ProteinsCell CommunicationEar, InnerHearing Loss, SensorineuralHumansKcnj10 ChannelPotassium Channels, Inwardly RectifyingSulfate TransportersAnionsAnion Transport ProteinsKcnj10 ChannelPotassium Channels, Inwardly RectifyingSlc26a4 protein, mouseSulfate Transporters

Identifiers

PMID22116367
PMCPMC7077107

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.