EC Number |
General Information |
Reference |
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3.4.22.38 | malfunction |
ablation of cathepsin K mitigates injury-induced neointimal hyperplasia. Smooth muscle cell movement is impaired in enzyme-deficient mice. Enzyme inhibition alleviates vascular remodeling. Enzyme deficiency also impairs the smooth muscle cell proliferation ability induced by platelet-derived growth factor-BB. Enzyme deficiency impairs inflammatory action in response to injury |
731902 |
3.4.22.38 | malfunction |
catK deficiency has major impact on various vasculopathies, catK deficiency does not protect against aneurysm formation nor does it affect medial elastin breaks, cathepsin K deficiency with angiotensin II infusion increases granulocyte population and activates T cell numbers |
707334 |
3.4.22.38 | malfunction |
down-regulation of cathepsin K in synovium at the initial stage of osteoarthritis significantly accelerates cartilage degeneration |
707318 |
3.4.22.38 | malfunction |
specific cathepsin K knockdown significantly reduces HSC-3 cell invasion in the myoma organotypic invasion model |
732741 |
3.4.22.38 | metabolism |
cathepsin K can cleave and activate MMP-9 in acidic environments such as seen in tumors and during bone resorption |
753109 |
3.4.22.38 | metabolism |
the enzyme accounts for the increase in bone resorption in metabolic bone disorders such as postmenopausal osteoporosis |
753907 |
3.4.22.38 | physiological function |
catepsin K is the key enzyme in bone homeostasis |
732842 |
3.4.22.38 | physiological function |
cathepsin K acts as the major collagenase responsible for the degradation of the organic bone matrix during the bone remodeling process |
708689 |
3.4.22.38 | physiological function |
cathepsin K expression is essential for normal bone resorption |
708580 |
3.4.22.38 | physiological function |
cathepsin K has a pivotal function in bone matrix degradation |
708260 |