EC Number   |
General Information |
Reference |
|---|
   3.4.24.24 | evolution |
MMP-2 is a member of the matrix metalloproteinase family |
752865 |
| 3.4.24.24 | malfunction |
in de novo formed fat pads, resulting from preadipocytes with Mmp2 knockdown, the expression of aP2, Ppar-gamma and adiponectin is significantly lower, and collagen is more preserved. The fat pad weights as well as size and density of adipocytes or blood vessels are not significantly different from controls, phenotype, overview |
-, 733414 |
| 3.4.24.24 | malfunction |
induction of diabetes in transgenic mice overexpressing human MMP2 show ignificant improvements in glycemia, glucose tolerance and insulin secretion compared to diabetic wild-type mice. Increased hMMP2 levels in mice correlate with significant reduction in islet beta-cell apoptosis compared to wild-type counterparts, and an inhibitor of hMMP2 reverses this mitigating activity against diabetes |
754619 |
| 3.4.24.24 | malfunction |
knockdown of LvMMP-2 expression decreases shrimp cumulative mortality upon oxidative stress. Knocked-down expression of LvMMP-2 depresse sthe expression of penaeidin2 and beta-defensin. Downregulation of LvMMP-2 suppresses the cumulative mortality of shrimp infected with white spot syndrome virus (WSSV) or with Vibrio alginolyticus |
753613 |
| 3.4.24.24 | malfunction |
the inactivation of the MMP-2 gene prevents thrombosis induced by weak, but not strong, stimuli but produces only a moderate prolongation of the bleeding time. MMP-2 deficient mice have hyporeactive platelets, a defective thrombotic response and mildly impaired hemostasis |
712613 |
| 3.4.24.24 | malfunction |
women with endometriosis show decreased MMP-2 activity in eutopic endometrium as compared to women without endometriosis, while ectopic ovarian endometrioma show significantly elevated MMP-2 activity with disease severity. Increased MMP-2 activation with disease progression |
755131 |
| 3.4.24.24 | metabolism |
aortic stiffness is an independent risk factor for development of cardiovascular diseases. Activation of renin-angiotensin-aldosterone system (RAAS) including angiotensin converting enzyme (ACE) activity leads to overproduction of angiotensin II (ANGII) from its precursor angiotensin I (ANGI). ANGII leads to overexpression and activation of matrix metalloproteinase-2 (MMP2), which is critically associated with pathophysiology of aortic stiffness |
754999 |
| 3.4.24.24 | metabolism |
evaluation of the effect that the hormonal fluctuations of the reproductive cycle have on the stromal remodeling and the expression and activity of matrix metalloproteinases MMP-2 and -9 in the adult female gerbil prostate, overview |
717633 |
| 3.4.24.24 | metabolism |
expansion of adipose tissue is dependent on adipogenesis, angiogenesis and extracellular matrix remodeling by the gelatinase subfamily of the matrix metalloproteinases, overview |
-, 733414 |
| 3.4.24.24 | more |
crucial role of the fibronectin-like domain in enzymatic activities, it is involved in substrate binding |
734343 |
