ArticleThe American journal of pathology2004
Keratinocytes from patients lacking collagen XVII display a migratory phenotype.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 123 citations in OpenAlex.
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- Native Autoantigen Complex Detects Pemphigoid Autoantibodies.JID innovations : skin science from molecules to population health · 2023Article
- Functional analysis of Collagen 17a1: A genetic modifier of junctional epidermolysis bullosa in mice.PloS one · 2023Article
- Junctional epithelium and hemidesmosomes: Tape and rivets for solving the "percutaneous device dilemma" in dental and other permanent implants.Bioactive materials · 2022Review
- Collagen XVII deficiency alters epidermal patterning.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Targeting the stem cell niche: role of collagen XVII in skin aging and wound repair.Theranostics · 2022Review
- BP180/Collagen XVII: A Molecular View.International journal of molecular sciences · 2021Review
- EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis.The Journal of cell biology · 2021Article
- Regulatory mechanism of oral mucosal rete peg formation.Journal of molecular histology · 2021Review
- A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.Antibodies (Basel, Switzerland) · 2021Review
- Multi-Omics Comparison of the Spontaneous Diabetes Mellitus and Diet-Induced Prediabetic Macaque Models.Frontiers in pharmacology · 2021Article
- Adenovirus-Mediated LAMA3 Transduction Enhances Hemidesmosome Formation and Periodontal Reattachment during Wound Healing.Molecular therapy. Methods & clinical development · 2020Article
- O-glycan initiation directs distinct biological pathways and controls epithelial differentiation.EMBO reports · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acquired or inherited junctional epidermolysis bullosa are skin diseases characterized by a separation between the epidermis and the dermis. In inherited nonlethal junctional epidermolysis bullosa, genetic analysis has identified mutations in the COL17A1 gene coding for the transmembrane collagen XVII whereas patients with acquired diseases have autoantibodies against this protein. This suggests that collagen XVII participates in the adhesion of basal keratinocytes to the extracellular matrix. To test this hypothesis, we studied the behavior of keratinocytes with null mutations in the COL17A1 gene. Initial adhesion of mutant cells to laminin 5 was comparable to controls and similarly dependent on alpha3beta1 integrins. The spreading of mutant cells was, however, enhanced, suggesting a propensity to migrate, which was confirmed by migration assays. In addition, laminin 5 deposited by collagen XVII-deficient keratinocytes was scattered and poorly organized, suggesting that correct integration of laminin 5 within the matrix requires collagen XVII. This assumption was supported by the co-distribution of the two proteins in the matrix of normal human keratinocytes and by protein-protein-binding assays showing that the C-terminus of collagen XVII binds to laminin 5. Together, the results unravel an unexpected role of collagen XVII in the regulation of keratinocyte migration.
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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.