Evidence map›Paper›PMID 36689403›Full record

ArticlePloS one2023

In-depth genetic and molecular characterization of diaphanous related formin 2 (DIAPH2) and its role in the inner ear.

Chiara Chiereghin, Michela Robusto, Morag A Lewis, Susana Caetano, Valentina Massa, Pierangela Castorina, Umberto Ambrosetti, Karen P Steel, Stefano Duga, Rosanna Asselta and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. 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
0.7field-weighted citation impact, top 29% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  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

11 authors at 6 institutions in 2 countries.

Chiara ChiereghinIRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.ORCID 0000-0002-7927-8317
Michela RobustoExperimental Therapeutics Program, IFOM ETS -The AIRC Institute of Molecular Oncology, Milan, Italy.
Morag A LewisWolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.ORCID 0000-0002-1846-8600
Susana CaetanoWolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.ORCID 0000-0003-2755-5404
Valentina MassaDipartimento di Scienze della Salute, Università degli Studi di Milano, Milano, Italy.
Pierangela CastorinaCasa di Cura Igea, Milano, Italy.
Umberto AmbrosettiDipartimento di Scienze Cliniche e di Comunità, Università degli Studi di Milano and Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, UO Audiologia, Milano, Italy.
Karen P SteelWolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.
Stefano DugaIRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
Rosanna AsseltaIRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
Giulia SoldàIRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.ORCID 0000-0003-0972-610X
Humanitas University · ITKing's College London · GBUniversity of Milan · ITCasa di Cura Columbus · ITIFOM · ITIRCCS Humanitas Research Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diaphanous related formins are regulatory cytoskeletal protein involved in actin elongation and microtubule stabilization. In humans, defects in two of the three diaphanous genes (DIAPH1 and DIAPH3) have been associated with different types of hearing loss. Here, we investigate the role of the third member of the family, DIAPH2, in nonsyndromic hearing loss, prompted by the identification, by exome sequencing, of a predicted pathogenic missense variant in DIAPH2. This variant occurs at a conserved site and segregated with nonsyndromic X-linked hearing loss in an Italian family. Our immunohistochemical studies indicated that the mouse ortholog protein Diaph2 is expressed during development in the cochlea, specifically in the actin-rich stereocilia of the sensory outer hair cells. In-vitro studies showed a functional impairment of the mutant DIAPH2 protein upon RhoA-dependent activation. Finally, Diaph2 knock-out and knock-in mice were generated by CRISPR/Cas9 technology and auditory brainstem response measurements performed at 4, 8 and 14 weeks. However, no hearing impairment was detected. Our findings indicate that DIAPH2 may play a role in the inner ear; further studies are however needed to clarify the contribution of DIAPH2 to deafness.

Indexed as

ActinsHearing LossAnimalsDeafnessForminsHair Cells, Auditory, OuterHumansMiceActinsDIAPH1 protein, humanDIAPH2 protein, humanFormins

Identifiers

PMID36689403
PMCPMC9870134
OpenAlexW4317780740

What OpenQuestion holds

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LicenceCC BY
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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.