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TIMP2 is a member of the TIMP gene family.
High TIMP2 expression is associated with chronic myelogenous leukemia.
No significant association was observed in MMP13 (show MMP13 Antibodies), TIMP2 and TGFB3 (show TGFB3 Antibodies) genes with CP or PI. CP is a risk factor to develop PI, however, there is no association of both diseases with polymorphisms in the MMP13 (show MMP13 Antibodies), TIMP2 and TGFB3 (show TGFB3 Antibodies) genes
MMP-2 (show MMP2 Antibodies) and TIMP-2 were secreted by both tumor cells and stromal cells.
miR (show MLXIP Antibodies)-22 significantly upregulated the invasion capacity of 1321N1 cells. In silico analysis predicted that TIMP2 is a target gene of miR (show MLXIP Antibodies)-22 which was confirmed by qPCR and Western blotting. Luciferase reporter assays demonstrated that miR (show MLXIP Antibodies)-22 directly bound the 3'-untranslated regions of TIMP2. These data suggest that miR (show MLXIP Antibodies)-22 acts to regulate invasion of 1321N1 astrocytoma cells by targeting TIMP2 expression.
TIMP-1 (show TIMP1 Antibodies) and-2 are primarily markers of an early function of the transplanted kidney.
Results show decreased expression of MMP-2 (show MMP2 Antibodies), MMP-9 (show MMP9 Antibodies) and TIMP-2 genes on both mRNA and protein levels in depression; there elevated expression positively affects cognitive efficiency.
TIMP- 2 expression decreased in cervical disc herniation patients.
significant differences were detected concerning the activity of TIMPs resulting in a negative correlation of TIMP1 (show TIMP1 Antibodies) activity with MMP2 (show MMP2 Antibodies) activity (p = 0.044) and negative correlations of TIMP2 and TIMP3 (show TIMP3 Antibodies) with MMP9 (show MMP9 Antibodies) activity
quantitative urine test is available to assess the risk of developing AKI by measuring the concentrations of two protein biomarkers, TIMP-2 and IGFBP-7 (show IGFBP7 Antibodies)
Here we report isothermal titration calorimetric studies of the effects of selectivity-modifying mutations in NTIMP1 and NTIMP2 on the thermodynamics of their interactions with MMP1 (show MMP1 Antibodies), MMP3 (show MMP3 Antibodies), and MMP14 (show MMP14 Antibodies).
Data indicate the involvement of PKC-alpha (show PKCa Antibodies) in proMMP-2 activation and inhibition of TIMP-2 expression by NF-kappaB (show NFKB1 Antibodies)-MT1-MMP (show MMP14 Antibodies)-dependent and -independent pathway.
A differential pattern of matrix metalloproteinase-2 (show MMP2 Antibodies) and Tissue inhibitor metalloproteinase-2 was observed in cow uteri with adenomyosis.
MMP-14 (show MMP14 Antibodies), MMP-2 (show MMP2 Antibodies) and TIMP-2 are co-localized in the fetal compartment and therefore could influence the timely release of fetal membranes in cattle.
Results describe distinct changes in expression of MMP2 (show MMP2 Antibodies), MMP14 (show MMP14 Antibodies), and the metallopeptidase (show ECEL1 Antibodies) inhibitor TIMP2 between different phases of the estrous cycle indicating an endocrine regulation.
Production of TIMP-1 (show TIMP1 Antibodies) was augmented by IL-1alpha, TNFalpha (show TNF Antibodies), and hepatocyte growth factor (show HGF Antibodies) at level of translation and was transcriptionally increased by 12-O-tetradecanoylphorbol 13-acetate. Level of TIMP-2 mRNA was not affected by any treatments.
the different temporal expression patterns of TIMP-1 (show TIMP1 Antibodies) and TIMP-2 suggest that TIMP-1 (show TIMP1 Antibodies) may be important for luteal formation and development, while TIMP-2 may play significant roles during luteal development and maintenance
Identification, purification and partial characterization of timp-2 in bovine pulmonary artery smooth muscle
Results describe the isolation of matrix metalloproteinase 2 (MMP-2 (show MMP2 Antibodies)) from the MMP-2 (show MMP2 Antibodies)/tissue inhibitor of metalloproteinase 2 (TIMP-2) complex, and the characterization of both isolated MMP-2 (show MMP2 Antibodies) and the complex itself.
oxidants inactivate TIMP-2, and the resulting activation of MMP-2 (show MMP2 Antibodies) subsequently inhibits Na+ dependent Ca2 (show CA2 Antibodies)+ uptake in the microsomes
TIMP-2 has a role in the pericyte-induced stabilization of newly formed vascular networks that are predisposed to undergo regression and reveal specific molecular targets of the inhibitors regulating these events.
demonstrate that TIMP-2 plays a greater protective role than TIMP-1 (show TIMP1 Antibodies) during the pathogenesis of atherosclerosis
Further investigation of MMP2 (show MMP2 Antibodies) inhibitors of TIMP2/TIMP4 (show TIMP4 Antibodies) showed an upregulated TIMP2 expression, but not TIMP4 (show TIMP4 Antibodies). low-dose pre-radiation attenuates the skin inflammation and ROS (show ROS1 Antibodies) production induced by medium-dose UV radiation
TIMP2 and TIMP3 (show TIMP3 Antibodies) play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function
Reduced beta(2)GP I plays a role in diabetic mice related to vascular protection, inhibiting vascular lipid deposition, and plaque formation by reducing MMPs/TIMPs expression through down-regulation of the p38MAPK (show MAPK14 Antibodies) signaling pathway.
High TIMP2 expression is associated with liver fibrosis.
TIMP2 promotes kidney injury through metalloproteinase (MMP)2 (show MMP2 Antibodies) activation
Gene expression of Mmp-12 (show MMP12 Antibodies) and Mmp-13 (show MMP13 Antibodies), and Timp-1 (show TIMP1 Antibodies) was strongly upregulated at all time points in RD compared with controls. Timp-2, Mmp-2 (show MMP2 Antibodies), and Mmp-9 (show MMP9 Antibodies) expression was modest.
Data indicate a significantly increased expression of type I collagen, TIMP-2, TGF-beta (show TGFB1 Antibodies), PAI-1 (show SERPINE1 Antibodies) and RAGE (show AGER Antibodies) in diabetic db/db (show LEPR Antibodies) cells.
This study suggests that miR-17 participates in the regulation of cardiac matrix remodeling and provides a novel therapeutic approach using miR-17 inhibitors to prevent remodeling and heart failure after MI.
In neural stem cells, TIMP-2 acts as key effector of the proneurogenic response to inducing stimuli such as Marimastat.
overexpression of TIMP-2 N- and C-terminal domains results in severe developmental defects and death, as well as unique changes in MMP-2 (show MMP2 Antibodies) and -9 expression, indicating that the individual domains may regulate MMPs through distinct mechanisms
characterization of Xenopus tissue inhibitor of metalloproteinases-2
This gene is a member of the TIMP gene family. The proteins encoded by this gene family are natural inhibitors of the matrix metalloproteinases, a group of peptidases involved in degradation of the extracellular matrix. In addition to an inhibitory role against metalloproteinases, the encoded protein has a unique role among TIMP family members in its ability to directly suppress the proliferation of endothelial cells. As a result, the encoded protein may be critical to the maintenance of tissue homeostasis by suppressing the proliferation of quiescent tissues in response to angiogenic factors, and by inhibiting protease activity in tissues undergoing remodelling of the extracellular matrix.
, metalloproteinase inhibitor 2
, tissue inhibitor of metalloproteinase 2
, tissue inhibitor of metalloproteinases 2
, tissue inhibitor of matrix metalloproteinase-2
, tissue inhibitor of metalloproteinase-2
, collagenase inhibitor
, tissue inhibitor of mettaloproteinase 2
, TIMP metallopeptidase inhibitor 2
, Metalloproteinase inhibitor 2