ArticleMatrix biology : journal of the International Society for Matrix Biology2019
Adamts10 inactivation in mice leads to persistence of ocular microfibrils subsequent to reduced fibrillin-2 cleavage.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 50 citations in OpenAlex.
- Review
- Current Advances in the Physiological Roles and Disease-Associated Mechanisms of ADAMTS16.International journal of molecular sciences · 2026Review
- The Pathogenic ADAMTSL2 D167N Variant Causes Geleophysic Dysplasia-Like Connective Tissue Changes in Mice.The American journal of pathology · 2026Article
- The ADAMTS family: from extracellular matrix proteases to orchestrators of fibrosis.Cell communication and signaling : CCS · 2026Review
- A novel homozygous ADAMTS10 frameshift variant in Weill-Marchesani syndrome in a Chinese family.BMC medical genomics · 2026Article
- An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and skin phenotypes.Life science alliance · 2025Article
- Kallikrein-8 mediates furin-independent Activin-A precursor processing to stimulate tumor growth in melanoma.Nature communications · 2025Article
- Review
- Review
- Screening of hub inflammatory bowel disease biomarkers and identification of immune-related functions based on basement membrane genes.European journal of medical research · 2023Article
- Role of elastic fiber degradation in disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Whole-exome sequencing prioritizes candidate genes for hereditary cataract in the Emory mouse mutant.G3 (Bethesda, Md.) · 2023Article
- A common variant rs2054564 in ADAMST17 is associated with susceptibility to lumbar spondylosis.Scientific reports · 2023Article
- Growth plate extracellular matrix defects and short stature in children.Annals of pediatric endocrinology & metabolism · 2022Article
- 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
- Article
- O-fucosylation of thrombospondin type 1 repeats is essential for ECM remodeling and signaling during bone development.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Adamts10 controls transforming growth factorFrontiers in molecular biosciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in the secreted metalloproteinase ADAMTS10 cause recessive Weill-Marchesani syndrome (WMS), comprising ectopia lentis, short stature, brachydactyly, thick skin and cardiac valve anomalies. Dominant WMS caused by FBN1 mutations is clinically similar and affects fibrillin-1 microfibrils, which are a major component of the ocular zonule. ADAMTS10 was previously shown to enhance fibrillin-1 assembly in vitro. Here, Adamts10 null mice were analyzed to determine the impact of ADAMTS10 deficiency on fibrillin microfibrils in vivo. An intragenic lacZ reporter identified widespread Adamts10 expression in the eye, musculoskeletal tissues, vasculature, skin and lung. Adamts10
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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.