Evidence map›Paper›PMID 25340345›Full record

ArticlePLoS genetics2014

Keratin 76 is required for tight junction function and maintenance of the skin barrier.

Tia DiTommaso, Denny L Cottle, Helen B Pearson, Holger Schlüter, Pritinder Kaur, Patrick O Humbert, Ian M Smyth

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Caspase-8-dependent autophagy regulates neutrophil infiltration in oral squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  18. Chitosan-Poly(caprolactone) Nanofibers for Skin Repair.Journal of materials chemistry. B · 2017
    Article
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Tia DiTommasoDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, Australia.
Denny L CottleDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, Australia.
Helen B PearsonResearch Division, The Sir Peter MacCallum Cancer Centre, Melbourne, Australia; The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia.
Holger SchlüterResearch Division, The Sir Peter MacCallum Cancer Centre, Melbourne, Australia; The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia.
Pritinder KaurResearch Division, The Sir Peter MacCallum Cancer Centre, Melbourne, Australia; The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia; Department of Anatomy & Neuroscience, University of Melbourne, Melbourne, Australia.
Patrick O HumbertResearch Division, The Sir Peter MacCallum Cancer Centre, Melbourne, Australia; The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia; Department of Biochemistry and Molecular Biology, University of Melbourne, Melbourne, Australia; Department of Pathology, University of Melbourne, Melbourne, Australia.
Ian M SmythDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, Australia; Department of Anatomy and Developmental Biology, Monash University, Melbourne, Australia.
Monash University · AUPeter MacCallum Cancer Centre · AUUniversity of Melbourne · AU

Funding

Wellcome Trust
6 · The paper itself

Abstract

Keratins are cytoskeletal intermediate filament proteins that are increasingly being recognised for their diverse cellular functions. Here we report the consequences of germ line inactivation of Keratin 76 (Krt76) in mice. Homozygous disruption of this epidermally expressed gene causes neonatal skin flaking, hyperpigmentation, inflammation, impaired wound healing, and death prior to 12 weeks of age. We show that this phenotype is associated with functionally defective tight junctions that are characterised by mislocalization of the integral protein CLDN1. We further demonstrate that KRT76 interacts with CLDN1 and propose that this interaction is necessary to correctly position CLDN1 in tight junctions. The mislocalization of CLDN1 has been associated in various dermopathies, including the inflammatory disease, psoriasis. These observations establish a previously unknown connection between the intermediate filament cytoskeleton network and tight junctions and showcase Krt76 null mice as a possible model to study aberrant tight junction driven skin diseases.

Indexed as

AnimalsClaudin-1CytoskeletonEpidermisHumansIntermediate FilamentsKeratinocytesKeratinsMicePsoriasisSkin DiseasesTight JunctionsClaudin-1Cldn1 protein, mouseKeratins

Identifiers

PMID25340345
PMCPMC4207637
OpenAlexW2052958748

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.