Target intelligence / Profile preview

ADAM metallopeptidase with thrombospondin type 1 motif 20 (ADAMTS20)

Target
ADAMTS20
Molecular classification
Enzyme (specifically, Zn2+-dependent metalloproteinase), Extracellular matrix proteinase, Secreted protein, ADAMTS (A disintegrin and metalloproteinase with thrombospondin motifs) family
01

Overview

ADAM metallopeptidase with thrombospondin type 1 motif 20 (ADAMTS20) is a member of the secreted ADAMTS family of zinc-dependent metalloproteases characterized by their modular structure, including multiple thrombospondin type 1 repeats. ADAMTS20 is primarily found in the extracellular matrix, where it participates in tissue remodeling by cleaving proteoglycans such as versican, contributing to processes like regression of interdigital webs and organogenesis. Recent findings also indicate a non-canonical role in ciliogenesis, where ADAMTS20, together with ADAMTS9, is involved in primary cilium formation and maintenance in specific cell types, likely impacting signaling pathways like Hedgehog. Mutations or inactivation in model organisms result in various developmental anomalies. No direct drug interactions, biomarker roles, or mechanisms of action in therapeutics have been established, but its functions suggest it may have future implications as a therapeutic target in fibrotic, developmental, or matrix-associated diseases[1][2][3][4][5].

Other names
ADAMTS-20ADAM-TS20GON-1ADAMTS20ADAM-TS 20a disintegrin and metalloproteinase with thrombospondin motifs 20
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Biological functions

Extracellular matrix organizationProteolysis (proteoglycan cleavage, e.g., versican)Tissue remodelingCiliogenesis regulationPossible role in intracellular trafficking of secretory cargos (GON domain associated)
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Disease associations

Developmental disorders (e.g., Peters-Plus Syndrome)Neurodevelopmental disorders with cerebellar atrophy and motor dysfunctionCraniofacial malformationsNeural tube defects(Research-stage) Ciliopathies and tissue morphogenesis anomalies
04

Safety considerations

Developmental defects when disrupted (in animal models, associated with craniofacial and neural tube anomalies)Potential off-target effects due to global tissue remodeling and extracellular matrix cleavage

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