Target intelligence / Profile preview

ADAM metallopeptidase with thrombospondin type 1 motif 14 (ADAMTS14)

Target
ADAMTS14
Molecular classification
Enzyme, Metalloprotease, Extracellular matrix protease
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Overview

ADAM metallopeptidase with thrombospondin type 1 motif 14 (ADAMTS14) is a secreted extracellular matrix protease and a member of the ADAMTS family, characterized by a signal peptide, a prodomain, a metalloprotease domain, a disintegrin-like domain, and a thrombospondin-1-like domain. It functions mainly in the processing of the amino-propeptides of fibrillar collagens, enabling collagen fibril formation prior to collagen assembly in the extracellular matrix. ADAMTS14 plays roles in ECM remodeling, cell migration, angiogenesis, and inflammation. Pathologically, it is implicated in osteoarthritis (by contributing to cartilage degradation), intervertebral disc disease, cancer progression (tumor invasion and angiogenesis), cardiovascular remodeling, and neurodegenerative diseases (neuroinflammation and neuronal damage)

Other names
A disintegrin and metalloprotease with thrombospondin motifs 14ADAMTS14ADAM-TS14ADAMTS-14ATS14A disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 14
02

Mechanism of action

Inhibition or modulation of proteolytic activity for prevention of ECM degradation, tumor growth, or inflammation (inferred from disease roles and biological functions since no specific drug listed)

03

Biological functions

Extracellular matrix (ECM) remodelingCleavage of amino-propeptides from fibrillar collagenCollagen fibril formationCell migrationAngiogenesisInflammation
04

Disease associations

OsteoarthritisIntervertebral disc diseaseCancerCardiovascular diseaseNeurodegenerative disorders
05

Safety considerations

Risk of impaired normal ECM remodeling if inhibitedPotential off-target effects in connective tissueRisk of impaired wound healing and angiogenesis if targeted
06

Biomarkers

Elevated ADAMTS14 levels in synovial fluid for osteoarthritis severityExpression changes in cancer, cardiovascular disease, and neurodegeneration (potential, not widely validated)

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