Evidence map›Paper›PMID 36936795›Full record

ArticleCurrent opinion in physiology2023

Mechanoelectrical transduction-related genetic forms of hearing loss.

Jinsei Jung, Ulrich Müller

Open access · greenAbstract read
In one paragraph

Article in Current opinion in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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

2 authors at 1 institution in 2 countries.

Jinsei JungThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ulrich MüllerThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Johns Hopkins University · US

Funding

Mechanosensor Development, Function, and DysfunctionR01DC005965 · NIDCD · SCRIPPS RESEARCH INSTITUTE, THE · PI MUELLER, ULRICH · 2003 to 2023
$10.2M
Integrative Structural and Functional Characterization of Tip-Link Cadherins DeafnessR01DC016960 · NIDCD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MUELLER, ULRICH, SHAPIRO, LAWRENCE S · 2018 to 2022
$3.3M
Mechanisms of Auditory Circuit DevelopmentR01DC019514 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI Ulrich Mueller · 2022 to 2026
$3.3M
NIDCD NIH HHS R01 DC005965NIDCD NIH HHS R01 DC016960NIDCD NIH HHS R01 DC019514
6 · The paper itself

Abstract

Hair cells of the mammalian cochlea are specialized mechanosensory cells that convert mechanical stimuli into electrical signals to initiate the neuronal responses that lead to the perception of sound. The mechanoelectrical transduction (MET) machinery of cochlear hair cells is a multimeric protein complex that consists of the pore forming subunits of the MET channel and several essential accessory subunits that are crucial to regulate channel function and render the channel mechanically sensitive. Mutations have been discovered in the genes that encode all known components of the MET machinery. These mutations cause hearing loss with or without vestibular dysfunction. Some mutations also affect other tissues such as the retina. In this brief review, we will summarize gene mutations that affect the MET machinery of hair cells and how the study of the affected genes has illuminated our understanding of the physiological role of the encoded proteins.

Indexed as

auditorydeafnesshair cellhearing lossmechanotransduction

Identifiers

PMID36936795
PMCPMC10022594
OpenAlexW4318020351

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.