EC Number   |
General Information |
Reference |
|---|
   3.4.24.35 | malfunction |
a truncated 65 kDa enzyme lacks the haemopexin domain required for the high-affinity binding of the tissue inhibitor TIMP-1, and can be evaluated by activity assay in the presence of tissue inhibitor of metalloproteinases 1, TIMP-1 |
734108 |
| 3.4.24.35 | malfunction |
administration of MMP-9 specific siRNA to the lungs of sensitized animals would abrogate development of an asthma phenotype, with endpoints of reduced airway hypersensitivity, less inflammation and tissue remodeling, less cellular migration of lymphocytes and eosinophils, and less activation of inflammatory cells, in both BAL fluids and lung tissues |
-, 733959 |
| 3.4.24.35 | malfunction |
enzyme inhibition prevents neural crest cells delamination and migration |
-, 733693 |
| 3.4.24.35 | malfunction |
in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis |
-, 734244 |
| 3.4.24.35 | malfunction |
in mice lacking MMP-9 the enhanced COX-1-PGE2 decreases caspase-3 expression and activity leading to impaired apoptosis of inflammatory neutrophils resulting in abnormal accumulation of the cells at the inflammatory focus |
708695 |
| 3.4.24.35 | malfunction |
increased levels of MMP-9 protein cause myopathy in dystrophin-deficient mdx mice. Deletion of Mmp9 gene in mdx mice improves skeletal muscle structure and functions and reduces muscle injury, inflammation and fiber necrosis. Heterozygous or homozygous deletion of MMP-9 attenuates accumulation of macrophages, fiber necrosis and improves force production in skeletal muscle of mdx mice. Genetic deletion of MMP-9 attenuates fibrosis in diaphragm of mdx mice. Genetic ablation of MMP-9 inhibits the activation of activator protein-1 and nuclear factor-kappaB transcription factors, reduces the serum level of creatine kinase and improves skeletal muscle structure in mdx mice. Genetic ablation of MMP-9 augments myofiber regeneration, improves sarcolemmal structure and augments the cellular levels of beta-dystroglycan and nNOS in skeletal muscle of mdx mice |
708653 |
| 3.4.24.35 | malfunction |
infection of chorioamniotic membranes with Escherichia coli induces an increase in the secretion of inactive forms and an association to extracellular matrix of active forms of MMP-2 and MMP-9 without changes in inhibitor TIMP-1, -2, and -4.These changes explain the significant decrease of collagen content and loss of structural continuity |
718385 |
| 3.4.24.35 | malfunction |
inhibition of matrix metalloproteinase-9 activity by doxycycline ameliorates RANK ligand-induced osteoclast differentiation in vitro and in vivo, overview. Doxycycline treatment abrogates RANKL-induced osteoclastogenesis and TRAP activity in mouse calvaria along with the suppression of MMP9 enzyme activity, again without affecting the expression of MMP9 protein |
-, 717577 |
| 3.4.24.35 | malfunction |
inhibition of MMP activity, especially MMP-9, has the potential to inhibit tumor growth and metastasis |
717980 |
| 3.4.24.35 | malfunction |
matrix metalloprotease-9 inhibition improves amyloid beta-mediated cognitive impairment and neurotoxicity in mice |
709680 |
