ArticlePloS one2012
The mechanical behavior of mutant K14-R125P keratin bundles and networks in NEB-1 keratinocytes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Sustained clinical remission of epidermolysis bullosa simplex due to a pathogenic KRT14 variant in a 7-year-old girl.JAAD case reports · 2026Article
- Pathological Mechanisms Involved in Epidermolysis Bullosa Simplex: Current Knowledge and Therapeutic Perspectives.International journal of molecular sciences · 2024Review
- Loss of keratin 14 expression from immortalized keratinocytes by promoter methylation.Experimental dermatology · 2024Article
- Quantitative mapping of keratin networks in 3D.eLife · 2022Article
- Plectin-mediated cytoskeletal crosstalk controls cell tension and cohesion in epithelial sheets.The Journal of cell biology · 2022Article
- Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021Review
- Cortical stiffness of keratinocytes measured by lateral indentation with optical tweezers.PloS one · 2020Article
- A rim-and-spoke hypothesis to explain the biomechanical roles for cytoplasmic intermediate filament networks.Journal of cell science · 2017Review
- Distinct Impact of Two Keratin Mutations Causing Epidermolysis Bullosa Simplex on Keratinocyte Adhesion and Stiffness.The Journal of investigative dermatology · 2015Article
- The expanding significance of keratin intermediate filaments in normal and diseased epithelia.Current opinion in cell biology · 2013Review
- Regulation of hard α-keratin mechanics via control of intermediate filament hydration: matrix squeeze revisited.Proceedings. Biological sciences · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Epidermolysis bullosa simplex (EBS) is an inherited skin-blistering disease that is caused by dominant mutations in the genes for keratin K5 or K14 proteins. While the link between keratin mutations and keratinocyte fragility in EBS patients is clear, the exact biophysical mechanisms underlying cell fragility are not known. In this study, we tested the hypotheses that mutant K14-R125P filaments and/or networks in human keratinocytes are mechanically defective in their response to large-scale deformations. We found that mutant filaments and networks exhibit no obvious defects when subjected to large uniaxial strains and have no negative effects on the ability of human keratinocytes to survive large strains. We also found that the expression of mutant K14-R125P protein has no effect on the morphology of the F-actin or microtubule networks or their responses to large strains. Disassembly of the F-actin network with Latrunculin A unexpectedly led to a marked decrease in stretch-induced necrosis in both WT and mutant cells. Overall, our results contradict the hypotheses that EBS mutant keratin filaments and/or networks are mechanically defective. We suggest that future studies should test the alternative hypothesis that keratinocytes in EBS cells are fragile because they possess a sparser keratin network.
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Registered trials
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.