Evidence map›Paper›PMID 41572507›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Compensatory Interplay Between Clarin-1 and Clarin-2 Deafness-Associated Proteins Governs Phenotypic Variability in Hearing.

Maureen Wentling, Aïda Yakhlef Sanchez, Nicolas Thelen, Müge Senarisoy, Maria Hogg, Steven Condamine, Andrea Lelli, Emilia Wysocka, Pranav Patni, Sandrine Vitry and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

18 authors.

Maureen WentlingInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Aïda Yakhlef SanchezInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Nicolas ThelenCellular and Tissular Biology, GIGA-Neurosciences, University of Liège, Liège, Belgium.
Müge SenarisoyInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Maria HoggInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Steven CondamineLaboratoire De Neurophysiologie de La Synapse Auditive, Institut De L'audition and Université de Bordeaux, Bordeaux, France.
Andrea LelliInstitut Pasteur, Institut De L'audition, AP-HP, INSERM, CNRS, Fondation Pour l'Audition, IHU reConnect, Auditory Therapies Innovation Laboratory, Université Paris Cité, Paris, France.
Emilia WysockaInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Pranav PatniInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Sandrine VitryInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Kerem Yasin YildizhanInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Sébastien Le GalInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Sylvie NouailleInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.
Michael R BowlUCL Ear Institute, University College London, London, UK.
Marc ThiryCollège Doctoral ED158, Sorbonne Université, Paris, France.
Didier DulonLaboratoire De Neurophysiologie de La Synapse Auditive, Institut De L'audition and Université de Bordeaux, Bordeaux, France.
Sedigheh DelmaghaniInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.ORCID https://orcid.org/0000-0003-2092-5097
Aziz El-AmraouiInstitut Pasteur, Institut De L'audition, AP-HP, INSERM U1335, CNRS, Fondation Pour l'Audition, IHU reConnect, Progressive Sensory Disorders, Pathophysiology and Therapy, Université Paris Cité, Paris, France.

Funding

Agence Nationale de la Recherche under the France 2030 Program ANR-23-IAHU-0003ANR-HearInNoise ANR-17-CE16-0017EuroNanoMed-NanoEar ANR-21-ENM3-0003-04European-Union's-Horizon 2020 Marie Sklodowska-Curie N°665807Fondation pour l'Audition FPA IDA07Fondation Recherche Médicale, Association Française contre les Myopathies AFM-TELETHON 29105Foundation Fighting Blindness PPA-0922-0840-INSERM
6 · The paper itself

Abstract

Usher syndrome type III (USH3) is a genetic disorder characterized by progressive, post-lingual hearing loss, variable vestibular dysfunction, and onset of retinitis pigmentosa. USH3 is caused by mutations in CLRN1, which encodes clarin-1, a tetraspanin-like protein. Mutations in CLRN2, which encodes the related protein clarin-2, are also implicated in progressive, non-syndromic hearing loss in both humans and mice. USH3 patients show considerable phenotypic variability, even among individuals with the same mutation. This variability may result from environmental factors or interactions with other inner ear genes, such as CLRN2. To investigate the functional interplay of these genes, we generated Clrn1

Indexed as

HearingMembrane ProteinsUsher SyndromesAnimalsDisease Models, AnimalHumansMiceMice, KnockoutMutationPhenotypeClrn1 protein, mouseMembrane ProteinsClarin‐1 and Clarin‐2hearing phenotypic variabilityion homeostasismechanoelectrical transductionsynaptopathyUsher syndrome type III

Identifiers

PMID41572507
PMCPMC13067776

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Registered trials

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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.