Evidence map›Paper›PMID 26915689›Full record

ArticleScientific reports2016

Distinct Expression Patterns Of Causative Genes Responsible For Hereditary Progressive Hearing Loss In Non-Human Primate Cochlea.

Makoto Hosoya, Masato Fujioka, Kaoru Ogawa, Hideyuki Okano

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Meta-Analysis ofGenes · 2019
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  6. Review
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  9. NIDCD's 5-Year Strategic Plan Describes Scientific Priorities and Commitment to Basic Science.Journal of the Association for Research in Otolaryngology : JARO · 2023
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  14. Review
  15. ARNSHL gene identification: past, present and future.Molecular genetics and genomics : MGG · 2022
    Review
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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

4 authors at 1 institution in 1 country.

Makoto HosoyaKeio University School of Medicine, Department of Otorhinolaryngology, Head and Neck Surgery, 35 Shinanomachi Shinjyuku-ku Tokyo, 160-8582, Japan.
Masato FujiokaKeio University School of Medicine, Department of Otorhinolaryngology, Head and Neck Surgery, 35 Shinanomachi Shinjyuku-ku Tokyo, 160-8582, Japan.
Kaoru OgawaKeio University School of Medicine, Department of Otorhinolaryngology, Head and Neck Surgery, 35 Shinanomachi Shinjyuku-ku Tokyo, 160-8582, Japan.
Hideyuki OkanoKeio University School of Medicine, Department of Physiology, 35 Shinanomachi Shinjyuku-ku Tokyo, 160-8582, Japan.
Keio University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hearing impairment is the most frequent sensory deficit in humans. Deafness genes, which harbor pathogenic mutations that have been identified in families with hereditary hearing loss, are commonly expressed in the auditory end organ or the cochlea and may contribute to normal hearing function, yet some of the mouse models carrying these mutations fail to recapitulate the hearing loss phenotype. In this study, we find that distinct expression patterns of those deafness genes in the cochlea of a non-human primate, the common marmoset (Callithrix jacchus). We examined 20 genes whose expression in the cochlea has already been reported. The deafness genes GJB3, CRYM, GRHL2, DFNA5, and ATP6B1 were expressed in marmoset cochleae in patterns different from those in mouse cochleae. Of note, all those genes are causative for progressive hearing loss in humans, but not in mice. The other tested genes, including the deafness gene COCH, in which mutation recapitulates deafness in mice, were expressed in a similar manner in both species. The result suggests that the discrepancy in the expression between rodents and primates may account for the phenotypic difference. This limitation of the rodent models can be bypassed by using non-human primate models such as the marmoset.

Indexed as

CallithrixCochleaHearing LossAmino Acid SequenceAnimalsConnexinsGene Expression ProfilingGenetic Predisposition to DiseaseImmunohistochemistryMice, Inbred C57BLmu-CrystallinsSequence Homology, Amino AcidSpecies SpecificityVacuolar Proton-Translocating ATPasesATP6V1C1 protein, humanConnexinsCRYM protein, humanCrym protein, mousemu-CrystallinsVacuolar Proton-Translocating ATPases

Identifiers

PMID26915689
PMCPMC4768099
OpenAlexW2365931658

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.