ReviewMatrix biology : journal of the International Society for Matrix Biology2015
ADAMTS proteins as modulators of microfibril formation and function.
Review in Matrix biology : journal of the International Society for Matrix Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 162 citations in OpenAlex.
- Review
- Deep Proteomic Analysis With Machine Learning Identifies Aqueous Humor Biomarkers of ADAMTSL4-associated Congenital Ectopia Lentis.Investigative ophthalmology & visual science · 2026Article
- Losartan shows limited benefit in preclinical models of Geleophysic dysplasia.Scientific reports · 2026Article
- Enhanced expression of ADAMTS1 in ovarian carcinomas: loss of ADAMTS1 expression instigates cellular reprogramming of extracellular matrix ensuing altered plasticity, augmented migration and attenuated adhesion.Journal of biomedical science · 2026Article
- Clinical and Surgical Implications of Genotype-Phenotype Correlations in Congenital Ectopia Lentis: A Real-World Cohort Study.Investigative ophthalmology & visual science · 2026Article
- Epigenetic dysregulation of IRF9 drives excessive interferon signaling in COPD.EMBO molecular medicine · 2026Article
- The ADAMTS family: from extracellular matrix proteases to orchestrators of fibrosis.Cell communication and signaling : CCS · 2026Review
- An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Keratinocyte self-renewal and differentiation is dictated by extrinsic signals from dermal extracellular matrices.Open biology · 2025Article
- The evolving genetic landscape of neuromuscular fetal akinesias.Journal of neuromuscular diseases · 2025Review
- Dysregulation of cell migration by matrix metalloproteinases in geleophysic dysplasia.Scientific reports · 2025Article
- Understanding Atherosclerotic Plaque Cellular Composition: Recent Advances Driven by Single Cell Omics.Cells · 2025Review
- THSD4 promotes hair growth by facilitating dermal papilla and hair matrix interactions.Theranostics · 2025Article
- Transcriptome analysis of the aortic coarctation area.Journal of molecular and cellular cardiology plus · 2024Article
- Trabecular Meshwork Abnormalities in a Model of Congenital Glaucoma Due to LTBP2 Mutation.Investigative ophthalmology & visual science · 2024Article
- From Atherosclerosis to Spontaneous Coronary Artery Dissection: Defining a Clinical and Genetic Risk Spectrum for Myocardial Infarction.Current atherosclerosis reports · 2024Review
- Article
- Integrative analyses of genetic characteristics associated with skeletal endothelial cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- A novel ADAMTSL4 compound heterozygous mutation in isolated ectopia lentis: a case report and review of the literature.Journal of medical case reports · 2023Review
- Advancements in the Genetics of Spontaneous Coronary Artery Dissection.Current cardiology reports · 2023Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ADAMTS (a disintegrin-like and metalloproteinase domain with thrombospondin-type 1 motifs) protein superfamily includes 19 secreted metalloproteases and 7 secreted ADAMTS-like (ADAMTSL) glycoproteins. The possibility of functional linkage between ADAMTS proteins and fibrillin microfibrils was first revealed by a human genetic consilience, in which mutations in ADAMTS10, ADAMTS17, ADAMTSL2 and ADAMTSL4 were found to phenocopy rare genetic disorders caused by mutations affecting fibrillin-1 (FBN1), the major microfibril component in adults. The manifestations of these ADAMTS gene disorders in humans and animals suggested that they participated in the structural and regulatory roles of microfibrils. Whereas two such disorders, Weill-Marchesani syndrome 1 and Weill-Marchesani-like syndrome involve proteases (ADAMTS10 and ADAMTS17, respectively), geleophysic dysplasia and isolated ectopia lentis in humans involve ADAMTSL2 and ADAMTSL4, respectively, which are not proteases. In addition to broadly similar dysmorphology, individuals affected by Weill-Marchesani syndrome 1, Weill-Marchesani-like syndrome or geleophysic dysplasia each show characteristic anomalies suggesting molecule-, tissue-, or context-specific functions for the respective ADAMTS proteins. Ectopia lentis occurs in each of these conditions except geleophysic dysplasia, and is due to a defect in the ciliary zonule, which is predominantly composed of FBN1 microfibrils. Together, this strongly suggests that ADAMTS proteins are involved either in microfibril assembly, stability, and anchorage, or the formation of function-specific supramolecular networks having microfibrils as their foundation. Here, the genetics and molecular biology of this subset of ADAMTS proteins is discussed from the perspective of how they might contribute to fully functional or function-specific microfibrils.
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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.