Evidence map›Paper›PMID 24751727›Full record

ArticleThe Journal of investigative dermatology2014

Loss of keratin K2 expression causes aberrant aggregation of K10, hyperkeratosis, and inflammation.

Heinz Fischer, Lutz Langbein, Julia Reichelt, Silke Praetzel-Wunder, Maria Buchberger, Minoo Ghannadan, Erwin Tschachler, Leopold Eckhart

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 49 citations in OpenAlex.

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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

8 authors at 3 institutions in 3 countries.

Heinz FischerDepartment of Dermatology, Medical University of Vienna, Vienna, Austria.
Lutz LangbeinDepartment of Genetics of Skin Carcinogenesis, German Cancer Research Center, Heidelberg, Germany.
Julia ReicheltInstitute of Cellular Medicine and North East England Stem Cell Institute, Newcastle University, Newcastle upon Tyne, UK.
Silke Praetzel-WunderDepartment of Genetics of Skin Carcinogenesis, German Cancer Research Center, Heidelberg, Germany.
Maria BuchbergerDepartment of Dermatology, Medical University of Vienna, Vienna, Austria.
Minoo GhannadanDepartment of Dermatology, Medical University of Vienna, Vienna, Austria.
Erwin TschachlerDepartment of Dermatology, Medical University of Vienna, Vienna, Austria.
Leopold EckhartDepartment of Dermatology, Medical University of Vienna, Vienna, Austria. Electronic address: leopold.eckhart@meduniwien.ac.at.
Medical University of Vienna · ATGerman Cancer Research Center · DENewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keratin K2 is one of the most abundant structural proteins of the epidermis; however, its biological significance has remained elusive. Here we show that suprabasal type II keratins, K1 and K2, are expressed in a mutually exclusive manner at different body sites of the mouse, with K2 being confined to the ear, sole, and tail skin. Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail epidermis, corneocyte fragility, increased transepidermal water loss, and local inflammation in the ear skin. The loss of K2 was partially compensated by upregulation of K1 expression. However, a significant portion of K2-deficient suprabasal keratinocytes lacked a regular cytoskeleton and developed massive aggregates of the type I keratin, K10. Aggregate formation, but not hyperkeratosis, was suppressed by the deletion of both K2 and K10, whereas deletion of K10 alone caused clumping of K2 in ear skin. Taken together, this study demonstrates that K2 is a necessary and sufficient binding partner of K10 at distinct body sites of the mouse and that unbalanced expression of these keratins results in aggregate formation.

Indexed as

AnimalsDermatitisDisease Models, AnimalEarFootHyperkeratosis, EpidermolyticKeratin-1Keratin-10Keratin-2MiceMice, Inbred C57BLMice, KnockoutSkinSkin DiseasesTailKeratin-1Keratin-10Keratin-2

Identifiers

PMID24751727
OpenAlexW2086607480

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.