ArticleThe Journal of biological chemistry2011
ADAMTS10 protein interacts with fibrillin-1 and promotes its deposition in extracellular matrix of cultured fibroblasts.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.
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Who cites it
85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 145 citations in OpenAlex.
- The American Association for Thoracic Surgery consensus guidelines on bicuspid aortic valve-related aortopathy: Full online-only version.The Journal of thoracic and cardiovascular surgery · 2018Guideline
- Bicuspid aortic valve aortopathy: genetics, pathophysiology and medical therapy.Interactive cardiovascular and thoracic surgery · 2013Pooled it
- 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
- Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and skin phenotypes.Life science alliance · 2025Article
- POGLUT2/3 mediated EGF O-glucosylation promotes separation of digits 2 and 3 by influencing fibrillin network reorganization, signaling, and cell dynamics.Developmental biology · 2025Article
- HSF2 drives breast cancer progression by acting as a stage-specific switch between proliferation and invasion.Science advances · 2025Article
- Kallikrein-8 mediates furin-independent Activin-A precursor processing to stimulate tumor growth in melanoma.Nature communications · 2025Article
- Review
- Review
- Adamts9 is required for the development of primary ovarian follicles and maintenance of female sex in zebrafish†.Biology of reproduction · 2024Article
- Expression Profiling ofIranian journal of public health · 2023Article
- Phylogenetic inference of the emergence of sequence modules and protein-protein interactions in the ADAMTS-TSL family.PLoS computational biology · 2023Article
- Role of fibrilins in human cancer: A narrative review.Health science reports · 2023Article
- Role of elastic fiber degradation in disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- A Novel Mutation in theInternational journal of molecular sciences · 2023Article
- A common variant rs2054564 in ADAMST17 is associated with susceptibility to lumbar spondylosis.Scientific reports · 2023Article
- ADAMTS10 inhibits aggressiveness via JAK/STAT/c-MYC pathway and reprograms macrophage to create an anti-malignant microenvironment in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Optic neuropathy associated with TGFβ dysregulation in mice with a glaucoma-causative mutation of ADAMTS10.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- The Mechanism and Role of ADAMTS Protein Family in Osteoarthritis.Biomolecules · 2022Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Autosomal recessive and autosomal dominant forms of Weill-Marchesani syndrome, an inherited connective tissue disorder, are caused by mutations in ADAMTS10 (encoding a secreted metalloprotease) and FBN1 (encoding fibrillin-1, which forms tissue microfibrils), respectively, yet they are clinically indistinguishable. This genetic connection prompted investigation of a potential functional relationship between ADAMTS10 and fibrillin-1. Specifically, fibrillin-1 was investigated as a potential ADAMTS10 binding partner and substrate, and the role of ADAMTS10 in influencing microfibril biogenesis was addressed. Using ligand affinity blotting and surface plasmon resonance, recombinant ADAMTS10 was found to bind to fibrillin-1 with a high degree of specificity and with high affinity. Two sites of ADAMTS10 binding to fibrillin-1 were identified, one toward the N terminus and another in the C-terminal half of fibrillin-1. Confocal microscopy and immunoelectron microscopy localized ADAMTS10 to fibrillin-1-containing microfibrils in human tissues. Furin-activated ADAMTS10 could cleave fibrillin-1, but innate resistance of ADAMTS10 zymogen to propeptide excision by furin was observed, suggesting that, unless activated, ADAMTS10 is an inefficient fibrillinase. To investigate the role of ADAMTS10 in microfibril biogenesis, fetal bovine nuchal ligament cells were cultured in the presence or absence of ADAMTS10. Exogenously added ADAMTS10 led to accelerated fibrillin-1 microfibril biogenesis. Conversely, fibroblasts obtained from a Weill-Marchesani syndrome patient with ADAMTS10 mutations deposited fibrillin-1 microfibrils sparsely compared with unaffected control cells. Taken together, these findings suggest that ADAMTS10 participates in microfibril biogenesis rather than in fibrillin-1 turnover.
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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.