ArticleProceedings of the National Academy of Sciences of the United States of America2025
LHFPL5 is required for maximal activation of the mechanotransduction channel in cochlear hair cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- PIPbioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Mechanoelectrical transduction (MET) channels in cochlear hair cells are gated by tip links through a mechanism that is poorly defined. LHFPL5 interacts with the tip-link component PCDH15 and the MET-channel component TMC1, suggesting that LHFPL5 regulates channel activation by mechanical force. To test this hypothesis, we analyzed MET in hair cells from mice expressing an LHFPL5 mutant protein lacking three N-terminal amino acids. These mutant mice suffer from recessive deafness, and MET is drastically impaired in cochlear hair cells. The resting open probability of the MET channels is increased in the mutants, while unitary channel conductance, adaptation, and tonotopic channel properties remain unaltered. Unlike in other LHFPL5 mutants, MET channel proteins are still present at normal levels in stereocilia of mutant mice. We conclude that LHFPL5 is required for maximal mechanical activation of MET channels in cochlear hair cells thereby affecting the hair bundle sensitivity to mechanical stimulation and thus the sound sensitivity of the auditory sense organ.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.