ArticleThe Journal of biological chemistry2009
Shedding of collagen XVII/BP180 in skin depends on both ADAM10 and ADAM9.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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.
Who cites it
44 citing papers in PubMed, 100 citations in OpenAlex.
- ADAM9 in tumor biology: molecular functions, clinical implications, and therapeutic targeting.Cellular & molecular biology letters · 2026Review
- Bullous Pemphigoid-Associated S aureus Increases Protease Activity from Keratinocytes and Promotes Unique BP180 Cleavage.The Journal of investigative dermatology · 2025Article
- IgG autoantibodies in bullous pemphigoid induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes.Nature communications · 2025Article
- Advances in Molecular Function and Recombinant Expression of Human Collagen.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Perturbation of EPHA2 and EFNA1iScience · 2025Article
- HeterozygousJournal of medical genetics · 2024Article
- Role of ADAM10 and ADAM17 in the Regulation of Keratinocyte Adhesion in Pemphigus Vulgaris.Frontiers in immunology · 2022Article
- ADAM10: Possible functions in enamel development.Frontiers in physiology · 2022Review
- Immunomodulatory role of metalloproteinase ADAM17 in tumor development.Frontiers in immunology · 2022Review
- Targeting the stem cell niche: role of collagen XVII in skin aging and wound repair.Theranostics · 2022Review
- Type XVII collagen: Relevance of distinct epitopes, complement-independent effects, and association with neurological disorders in pemphigoid disorders.Frontiers in immunology · 2022Review
- Crucial Roles of microRNA-16-5p and microRNA-27b-3p in Ameloblast Differentiation Through Regulation of Genes Associated With Amelogenesis Imperfecta.Frontiers in genetics · 2022Article
- 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
- Collagen Biosynthesis, Processing, and Maturation in Lung Ageing.Frontiers in medicine · 2021Review
- Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth.Biomolecules · 2020Article
- Collagen XVII Processing and Blistering Skin Diseases.Acta dermato-venereologica · 2020Review
- Prominence of IL6, IGF, TLR, and Bioenergetics Pathway Perturbation in Lung Tissues of Scleroderma Patients With Pulmonary Fibrosis.Frontiers in immunology · 2020Article
- The Role of Collagen XVII in Cancer: Squamous Cell Carcinoma and Beyond.Frontiers in oncology · 2020Review
- Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Collagen XVII is a transmembrane collagen and the major autoantigen of the autoimmune skin blistering disease bullous pemphigoid. Collagen XVII is proteolytically released from the membrane, and the pathogenic epitope harbors the cleavage site for its ectodomain shedding, suggesting that proteolysis has an important role in regulating the function of collagen XVII in skin homeostasis. Previous studies identified ADAMs 9, 10, and 17 as candidate collagen XVII sheddases and suggested that ADAM17 is a major sheddase. Here we show that ADAM17 only indirectly affects collagen XVII shedding and that ADAMs 9 and 10 are the most prominent collagen XVII sheddases in primary keratinocytes because (a) collagen XVII shedding was not stimulated by phorbol esters, known activators of ADAM17, (b) constitutive and calcium influx-stimulated shedding was sensitive to the ADAM10-selective inhibitor GI254023X and was strongly reduced in Adam10(-/-) cells, (c) there was a 55% decrease in constitutive collagen XVII ectodomain shedding from Adam9(-/-) keratinocytes, and (d) H(2)O(2) enhanced ADAM9 expression and stimulated collagen XVII shedding in skin and keratinocytes of wild type mice but not of Adam9(-/-) mice. We conclude that ADAM9 and ADAM10 can both contribute to collagen XVII shedding in skin with an enhanced relative contribution of ADAM9 in the presence of reactive oxygen species. These results provide critical new insights into the identity and regulation of the major sheddases for collagen XVII in keratinocytes and skin and have implications for the treatment of blistering diseases of the skin.
Indexed as
Identifiers
What OpenQuestion holds
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.