EC Number   |
General Information |
Reference |
|---|
   3.4.24.82 | malfunction |
aortas in enzyme-deficient mice show reduced elastic fibre destruction, versican degradation, macrophage infiltration, and apoptosis. Enzyme deficiency in mice partially prevents aortic destruction and proteoglycan degradation, decreases inflammatory cell infiltration in the aorta, and reduces aortic apoptosis |
755457 |
| 3.4.24.82 | malfunction |
the lack of hevin cleavage, as seen in ADAMTS4-null mice results in altered Purkinje-cell morphology and a reactive gliosis phenotype in the brain of these adult animals |
709151 |
| 3.4.24.82 | physiological function |
ADAMTS-4 digests proteoglycans, and reverses their inhibition of neurite outgrowth. Local administration of ADAMTS-4 significantly promotes motor function recovery after spinal cord injury. The ADAMTS-4-treated spinal cord exhibits enhanced axonal regeneration/sprouting after spinal cord injury |
734526 |
| 3.4.24.82 | physiological function |
ADAMTS-4 inhibits human dermal microvascular endothelial cells (HuDMEC) vascular endothelial growth factor-stimulated vascular endothelial growth factor receptor R2 phosphorylation in a dose-related manner to give a maximum of about 65% inhibition at and above 30 nM. ADAMTS-4 reduces HuDMEC differentiation and migration |
719609 |
| 3.4.24.82 | physiological function |
ADAMTS-4 is responsible for aggrecan degradation during human articular cartilage destruction in vivo |
720093 |
| 3.4.24.82 | physiological function |
both long and short forms of the procollagen C-proteinase enhancers netrin-like (PCPE-1 NTR) domain show no inhibition, at micromolar concentrations, of several members of the metzincin superfamily, including matrix metalloproteinase-2, bone morphogenetic protein-1, and different ADAMTS-2, ADAMTS-4 or ADAMTS-5 |
707442 |
| 3.4.24.82 | physiological function |
disruptive changes in chondrocyte-matrix interactions by hyaluran oligosaccharides induce matrix degradation and elevate aggrecanases ADAMTS4, ADAMTS5 via the activation of the NF-kappaB signaling pathway |
733229 |
| 3.4.24.82 | physiological function |
fibulin-2 degradation by the enzyme is associated to an enhancement of the invasive potential of T-47D, MCF-7 and SK-BR-3 breast cancer cells |
754958 |
| 3.4.24.82 | physiological function |
full-length ADAMTS4 and its catalytically more active N-terminal 53 kDa autocatalytic fragment both promote B16 melanoma growth and angiogenesis in mice. Overexpression of its catalytically inactive E362A mutant or truncated fragments containing only the C-terminal ancillary domains suppresses melanoma growth and angiogenesis under similar conditions. The single thrombospondin-type 1 repeat domain is essential and sufficient for the antitumorigenic activity of the catalytically inactive ADAMTS4 isoforms. Suppression of tumor growth and angiogenesis in mice is accompanied by a significant increase in tumor cell apoptosis, whereas tumor cell proliferation is not affected |
733990 |
| 3.4.24.82 | physiological function |
the enzyme contributes to aortic destruction and sporadic aortic aneurysm and dissection development and is directly involved in smooth muscle cell apoptosis |
755457 |
