Associated Papers
Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and skin phenotypes.
Taye N et al.
Life Science Alliance, 2025
Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and compromises extracellular matrix formation.
Taye N et al.
Biorxiv : the Preprint Server for Biology, 2025
Zonulopathies as Genetic Disorders of the Extracellular Matrix.
Chipeta C et al.
Genes, 2024
Exome sequencing (ES) of a pediatric cohort with chronic endocrine diseases: a single-center study (within the framework of the TRANSLATE-NAMSE project).
Gippert S et al.
Endocrine, 2024
The ADAMTS/Fibrillin Connection: Insights into the Biological Functions of ADAMTS10 and ADAMTS17 and Their Respective Sister Proteases.
Karoulias SZ et al.
Biomolecules, 2020
Genomic Landscape and Mutational Spectrum of ADAMTS Family Genes in Mendelian Disorders Based on Gene Evidence Review for Variant Interpretation.
Rim JH et al.
Biomolecules, 2020
ADAMTS10-mediated tissue disruption in Weill-Marchesani syndrome.
Mularczyk EJ et al.
Human Molecular Genetics, 2018
Homozygous mutations in ADAMTS10 and ADAMTS17 cause lenticular myopia, ectopia lentis, glaucoma, spherophakia, and short stature.
Morales J et al.
American Journal of Human Genetics, 2009
ADAMTS10 mutations in autosomal recessive Weill-Marchesani syndrome.
Dagoneau N et al.
American Journal of Human Genetics, 2004
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