EC Number |
Application |
Reference |
---|
3.4.24.82 | degradation |
degradation of cartilage in late-stage Lyme arthritis |
-, 667360 |
3.4.24.82 | degradation |
abrasion of cartilage aggrecan in rheumatoid arthritis and osteoarthritis |
667796 |
3.4.24.82 | degradation |
degradation of cartilage proteoglycan (aggrecan) in osteoarthritis and rheumatoid arthritis |
669244 |
3.4.24.82 | medicine |
therapeutic target in osteoarthritis |
679302 |
3.4.24.82 | medicine |
stop progression of cartilage degradation in osteoarthritis by prevention of aggrecan cleavage via inhibition of aggrecanase-1 |
696674 |
3.4.24.82 | more |
neurite extension mediated by the MAP kinase pathway, increased number of primary and secondary neurites |
697804 |
3.4.24.82 | medicine |
the pattern of ADAMTS4 release observed is clearly different in various forms of ACS. ADAMTS4 shows a weak correlation with high-sensitivity C-reactive protein. However, no significant correlation is found between ADAMTS4 and troponin T in acute coronary syndromes patients |
707655 |
3.4.24.82 | medicine |
design and development for potent and selective inhibitors of ADAMTS-4 and ADAMTS-5, which will be required for chronic osteoarthritis therapy |
709044 |
3.4.24.82 | medicine |
ADAMTS-4 is a key enzyme in osteoarthritis |
720093 |
3.4.24.82 | medicine |
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 |