Evidence map›Paper›PMID 22895363›Full record

ArticleThe Journal of investigative dermatology2013

Keratins mediate localization of hemidesmosomes and repress cell motility.

Kristin Seltmann, Wera Roth, Cornelia Kröger, Fanny Loschke, Marcell Lederer, Stefan Hüttelmaier, Thomas M Magin

Abstract read
In one paragraph

Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. HMCN1 variants aggravate epidermolysis bullosa simplex phenotype.The Journal of experimental medicine · 2025
    Article
  3. Article
  4. Keratin isoform shifts modulate motility signals during wound healing.bioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

7 authors at 2 institutions in 1 country.

Kristin SeltmannInstitute of Biology, University of Leipzig, Leipzig, Germany.
Wera Roth
Cornelia Kröger
Fanny Loschke
Marcell Lederer
Stefan Hüttelmaier
Thomas M Magin
Leipzig University · DEMartin Luther University Halle-Wittenberg · DE

Funding

Montagna Symposium on the Biology of SkinR13AR009431 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SANCY ANN LEACHMAN · 1986 to 2026
$785k
NIAMS NIH HHS R13 AR009431
6 · The paper itself

Abstract

The keratin (K)-hemidesmosome (HD) interaction is crucial for cell-matrix adhesion and migration in several epithelia, including the epidermis. Mutations in constituent proteins cause severe blistering skin disorders by disrupting the adhesion complex. Despite extensive studies, the role of keratins in HD assembly and maintenance is only partially understood. Here we address this issue in keratinocytes in which all keratins are depleted by genome engineering. Unexpectedly, such keratinocytes maintain many characteristics of their normal counterparts. However, the absence of the entire keratin cytoskeleton leads to loss of plectin from the hemidesmosomal plaque and scattering of the HD transmembrane core along the basement membrane zone. To investigate the functional consequences, we performed migration and adhesion assays. These revealed that, in the absence of keratins, keratinocytes adhere much faster to extracellular matrix substrates and migrate approximately two times faster compared with wild-type cells. Reexpression of the single keratin pair K5 and K14 fully reversed the above phenotype. Our data uncover a role of keratins, which to our knowledge is previously unreported, in the maintenance of HDs upstream of plectin, with implications for epidermal homeostasis and pathogenesis. They support the view that the downregulation of keratins observed during epithelial-mesenchymal transition supports the migratory and invasive behavior of tumor cells.

Indexed as

Cell MovementAnimalsBasement MembraneCells, CulturedCytoskeletonExtracellular MatrixHemidesmosomesKeratin-14Keratin-15Keratin-5KeratinocytesKeratinsMiceMice, KnockoutPlectinKeratin-14Keratin-15Keratin-5KeratinsKrt14 protein, mouseKrt15 protein, mousePlec protein, mousePlectin

Identifiers

PMID22895363
PMCPMC3575009
OpenAlexW1973137441

What OpenQuestion holds

Textmetadata
LicenceTDM
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.