Evidence map›Paper›PMID 25063198›Full record

ArticleBiology open2014

Deafness in occludin-deficient mice with dislocation of tricellulin and progressive apoptosis of the hair cells.

Shin-Ichiro Kitajiri, Tatsuya Katsuno, Hiroyuki Sasaki, Juichi Ito, Mikio Furuse, Shoichiro Tsukita

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  6. The ethanolic extract of domesticatedFood science and biotechnology · 2024
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  7. Article
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  9. A short guide to the tight junction.Journal of cell science · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Serine 408 phosphorylation is a molecular switch that regulates structure and function of the occludin α-helical bundle.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Review
  16. Article
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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

6 authors at 3 institutions in 1 country.

Shin-Ichiro KitajiriDepartment of Otolaryngology, Head and Neck Surgery, Kyoto University Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan kitajiri@ent.kuhp.kyoto-u.ac.jp.
Tatsuya KatsunoDepartment of Otolaryngology, Head and Neck Surgery, Kyoto University Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
Hiroyuki SasakiDepartment of Physical Therapy, Faculty of Community Health Care, Teikyo Heisei University, Uruido Minami, Ichihara, Chiba 290-0193, Japan.
Juichi ItoDepartment of Otolaryngology, Head and Neck Surgery, Kyoto University Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
Mikio FuruseDepartment of Cell Biology, Division of Cell Biology, Kobe University Graduate School of Medicine, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan Division of Cerebral Structure, National Institute for Physiological Sciences, Okazaki, 444-8787, Japan.
Shoichiro TsukitaDepartment of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
Kyoto University · JPNational Institute for Physiological Sciences · JPTeikyo Heisei University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Occludin is the first identified protein in the tight junction (TJ), but its function has remained for the most part obscure. TJs have been demonstrated to play important roles in the inner ear function, and occludin is expressed in all the epithelial TJs in the inner ear. Thus, we examined the inner ears of occludin-deficient (Occ(-/-)) mice. Although inner ears initially developed normally in Occ(-/-) mice, apoptosis occurs in hair cells in the organ of Corti around day 12 after birth, and deafness develops. Since hair cell degeneration was not observed in cochlear explant cultures of Occ(-/-) mice, environmental changes were considered to be the trigger of cell death. As for the vestibular system, both the morphologies and functions are normal in Occ(-/-) mice. These phenotypes of Occ(-/-) mice are very similar with those of claudin-14 or claudin-9 deficient mice, leading us to speculate on the existence of imbalance induced by TJ abnormalities, such as localized ionic components. Moreover, the occludin deficiency led to dislocalization of tricellulin, a gene responsible for human deafness DFNB49. The deafness in Occ(-/-) mice may be due to this dislocalization of tricellulin.

Indexed as

CochleaDeafnessHair cellOccludinTight junctionTricellulin

Identifiers

PMID25063198
PMCPMC4133728
OpenAlexW2110114499

What OpenQuestion holds

Textmetadata
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.