EC Number   |
General Information |
Reference |
|---|
   3.4.24.B12 | malfunction |
ADAMTS-5 deficient mice do not develop mechanical allodynia associated with osteoarthritis following medial meniscal destabilization |
710191 |
| 3.4.24.B12 | malfunction |
ADAMTS-5 knockout mice express no major phenotypical abnormalities, but show a significant reduction in the severity of surgically induced osteoarthritis in the ADAMTS-5 in contrast to the ADAMTS-4 knockout groups |
720093 |
| 3.4.24.B12 | malfunction |
ADAMTS5 deficient mice have reduced versican proteolysis, increased pericellular matrix, altered cell shape, enhanced alpha-smooth muscle actin expression and increased contractility within three dimensional collagen gels |
719966 |
| 3.4.24.B12 | malfunction |
ADAMTS5-/- mice have significantly less cartilage damage than wild-type after induction of osteoarthritis through surgical instability |
710190 |
| 3.4.24.B12 | malfunction |
enzyme-deficient mice develop less subcutaneous and gonadal white adipose tissue as compared to their wild type littermates. Enhanced browning of white adipose tissue and improved insulin sensitivity are seen in enzyme-knockout mice upon cold exposure |
755160 |
| 3.4.24.B12 | malfunction |
influenza virus infection of enzyme-deficient mice results in delayed virus clearance, compromised T cell migration and immunity and accumulation of versican. Enzyme-deficient mice exhibit increased weight loss and delayed influenza virus clearance following infection |
755055 |
| 3.4.24.B12 | malfunction |
insufficiency of enzyme expression in Sertoli cells may have an important role in the etiology of male infertility |
755570 |
| 3.4.24.B12 | malfunction |
skeletal muscle formation is disrupted in enzyme-deficient embryos |
753919 |
| 3.4.24.B12 | physiological function |
ADAMTS-5 contributes to the structural damage of cartilage that characterizes human osteoarthritis |
720093 |
| 3.4.24.B12 | physiological function |
ADAMTS-5 is markedly reduced in atherosclerotic aortas of apolipoprotein E-null mice. The reduction of ADAMTS-5 is accompanied by accumulation of biglycan and versican, the major lipoprotein-binding proteoglycans, in atherosclerosis. ADAMTS-5 activity induced the release of ADAMTS-specific versican and aggrecan fragments as well as biglycan and link protein from the aortic wall. Fibroblast growth factor 2 inhibits ADAMTS-5 expression in isolated aortic smooth muscle cells and blocked the spontaneous release of ADAMTS-generated versican and aggrecan fragments from aortic explants. In aortas of ADAMTS-5-deficient mice, ADAMTS-specific versican neoepitopes are not detectable. Biglycan levels are increased. ADAMTS-5 proteolytic activity reduces the low density lipoprotein binding ability of biglycan and releases low density lipoprotein from human aortic lesions |
734180 |
