Evidence map›Paper›PMID 25668239›Full record

ArticleThe Journal of investigative dermatology2015

Keratins Stabilize Hemidesmosomes through Regulation of β4-Integrin Turnover.

Kristin Seltmann, Fang Cheng, Gerhard Wiche, John E Eriksson, Thomas M Magin

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. HMCN1 variants aggravate epidermolysis bullosa simplex phenotype.The Journal of experimental medicine · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Diacetyl inhalation impairs airway epithelial repair in mice infected with influenza A virus.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Desmin Modulates Muscle Cell Adhesion and Migration.Frontiers in cell and developmental biology · 2022
    Article
  13. Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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

5 authors at 4 institutions in 3 countries.

Kristin SeltmannTRM Leipzig & Institute of Biology, Division of Cell and Developmental Biology, University of Leipzig, Leipzig, Germany.
Fang ChengDepartment of Biosciences and Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Gerhard WicheDepartment of Biochemistry and Cell Biology, Max F, Perutz Laboratories, University of Vienna, Vienna, Austria.
John E ErikssonDepartment of Biosciences and Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Thomas M MaginTRM Leipzig & Institute of Biology, Division of Cell and Developmental Biology, University of Leipzig, Leipzig, Germany. Electronic address: thomas.magin@trm.uni-leipzig.de.
Leipzig University · DEÅbo Akademi University · FITurku Centre for Biotechnology · FIUniversity of Vienna · AT

Funding

Austrian Science Fund FWF I 1207Austrian Science Fund FWF P 23729
6 · The paper itself

Abstract

Epidermal integrity and wound healing depend on remodeling of cell-matrix contacts including hemidesmosomes. Mutations in β4-integrin and plectin lead to severe epidermolysis bullosa (EB). Whether mutations in keratins K5 or K14, which cause EB simplex, also compromise cell-matrix adhesion through altering hemidesmosomal components is not well investigated. In particular, the dependence of β4-integrin endocytosis and turnover on keratins remains incompletely understood. Here, we show that the absence of keratins causes loss of plectin-β4-integrin interaction and elevated β4-integrin phosphorylation at Ser1354 and Ser1362. This triggered a caveolin-dependent endocytosis of β4-integrin but not of other integrins through Rab5 and Rab11 compartments in keratinocytes. Expressing a phospho-deficient β4-integrin mutant reduces β4-integrin endocytosis and rescues plectin localization in keratin-free cells. β4-integrin phosphorylation in the absence of keratins resulted from elevated Erk1/2 activity downstream of increased EGFR and PKCα signaling. Further, increased Erk1/2 phosphorylation and altered plectin localization occur in keratin-deficient mouse epidermis in vivo. Strikingly, expression of the K14-R125P EBS mutant also resulted in plectin mislocalization and elevated β4-integrin turnover, suggesting disease relevance. Our data underscore a major role of keratins in controlling β4-integrin endocytosis involving a plectin-Erk1/2-dependent mechanism relevant for epidermal differentiation and pathogenesis.

Indexed as

Gene Expression RegulationAnimalsCaveolinsCell SeparationEndocytosisEpidermisErbB ReceptorsFlow CytometryFluorescence Recovery After PhotobleachingGenotypeHemidesmosomesIntegrin beta4KeratinocytesKeratinsLasersMiceCaveolinsErbB ReceptorsIntegrin beta4KeratinsPlectinProtein Kinase C-alpharab11 GTP-Binding Proteinsrab5 GTP-Binding Proteinsrab GTP-Binding ProteinsSerine

Identifiers

PMID25668239
OpenAlexW2014880437

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.