Evidence map›Paper›PMID 18436651›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Targeted deletion of the murine corneodesmosin gene delineates its essential role in skin and hair physiology.

Mitsuru Matsumoto, Yiqing Zhou, Shinji Matsuo, Hideki Nakanishi, Kenji Hirose, Hajimu Oura, Seiji Arase, Akemi Ishida-Yamamoto, Yoshimi Bando, Keisuke Izumi and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Deletion of the Epidermal ProteaseInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Loricrin and NRF2 Coordinate Cornification.JID innovations : skin science from molecules to population health · 2022
    Article
  12. The Epidermis: Redox Governor of Health and Diseases.Antioxidants (Basel, Switzerland) · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

19 authors at 6 institutions in 2 countries.

Mitsuru MatsumotoDivision of Molecular Immunology, Institute for Enzyme Research, University of Tokushima, Tokushima 770-8503, Japan. mitsuru@ier.tokushima-u.ac.jp
Yiqing Zhou
Shinji Matsuo
Hideki Nakanishi
Kenji Hirose
Hajimu Oura
Seiji Arase
Akemi Ishida-Yamamoto
Yoshimi Bando
Keisuke Izumi
Hiroshi Kiyonari
Naoko Oshima
Rika Nakayama
Akemi Matsushima
Fumiko Hirota
Yasuhiro Mouri
Noriyuki Kuroda
Shigetoshi Sano
David D Chaplin
Tokushima University · JPGenetic Resources Center · JPAsahikawa Medical College Hospital · JPKōchi University · JPTokushima University Hospital · JPUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Controlled proteolytic degradation of specialized junctional structures, corneodesmosomes, by epidermal proteases is an essential process for physiological desquamation of the skin. Corneodesmosin (CDSN) is an extracellular component of corneodesmosomes and, although considerable debate still exists, genetic studies have suggested that the CDSN gene in the major psoriasis-susceptibility locus (PSORS1) may be responsible for susceptibility to psoriasis, a human skin disorder characterized by excessive growth and aberrant differentiation of keratinocytes. CDSN is also expressed in the inner root sheath of hair follicles, and a heterozygous nonsense mutation of the CDSN gene in humans is associated with scalp-specific hair loss of poorly defined etiology. Here, we have investigated the pathogenetic roles of CDSN loss of function in the development of skin diseases by generating a mouse strain with targeted deletion of the Cdsn gene. Cdsn-deficient mouse skin showed detachment of the stratum corneum from the underlying granular layer and/or detachment within the upper granular layers due to the disrupted integrity of the corneodesmosomes. When grafted onto immunodeficient mice, Cdsn-deficient skin showed rapid hair loss together with epidermal abnormalities resembling psoriasis. These results underscore the essential roles of CDSN in hair physiology and suggest functional relevance of CDSN gene polymorphisms to psoriasis susceptibility.

Indexed as

Gene DeletionGene TargetingAnimalsDesmosomesGlycoproteinsHairMicePhenotypePsoriasisSkin AbnormalitiesSkin Physiological PhenomenaSkin Transplantationcorneodesmosin protein, mouseGlycoproteins

Identifiers

PMID18436651
PMCPMC2373361
OpenAlexW2062805185

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.