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TIMP3 belongs to the TIMP gene family. Additionally we are shipping TIMP3 Antibodies (215) and TIMP3 Kits (98) and many more products for this protein.
Showing 10 out of 17 products:
TIMP3 methylation is a marker for TN tumours and furthermore we showed for the first time that TIMP3 promoter methylation is an epigenetic marker of BRCA1ness tumours.
As a novel CLOCK-dependent diurnal gene, TIMP3 inhibits the expression of inflammatory cytokines that are up-regulated by UV irradiation in human keratinocytes.
miR (show MLXIP Proteins)-21-5p mediates apoptosis by targeting PTEN and TIMP3.
Preliminary studies indicate that baseline MMP3 (show MMP3 Proteins) and TIMP3 concentrations are associated with patient survival and disease-free time
TIMP-3 mRNA expression levels positively correlates with levels of miR (show MLXIP Proteins)-21 in in situ breast carcinomas and negatively in progesterone receptor (show PGR Proteins) positive invasive breast carcinomas.
Sphingosine-1-phosphate inhibited cell migration and MMP-2 (show MMP2 Proteins) expression through the upregulation of the tissue inhibitor of metalloproteinase-3 (TIMP-3) expression in human chondrosarcoma cells.
Using global proteomic profiling of brain leptomeningeal arteries, this study revealed that clusterin (show CLU Proteins) and tissue inhibitor of metalloproteinases-3 increase in leptomeningeal arteries affected by cerebral amyloid angiopathy.
This is the first report of a syndromic Sorsby fundus dystrophy in line with the mouse model uncovering the role of TIMP3 in human lung morphogenesis and functions.
Collectively, these results demonstrated that IL-32alpha upregulates the atheroprotective genes Timp3 and Reck (show RECK Proteins) by downregulating microRNA-205 through regulation of the Rprd2-Dgcr8 (show DGCR8 Proteins)/Ddx5 (show DDX5 Proteins)-Dicer1 (show DICER1 Proteins) biogenesis pathway.
MMP-13 (show MMP13 Proteins) may play a role on physiological turnover of cartilage extracellular matrix and that LRP1 (show LRP1 Proteins) is a key modulator of extracellular levels of MMP-13 (show MMP13 Proteins) and its internalization is independent of the levels of ADAMTS-4 (show ADAMTS4 Proteins), -5 and TIMP-3.
The present study demonstrated the ability of 30 and 100 ng/ml TIMP3 to attenuate migration and proliferation, and to inhibit the activity of MMP2 (show MMP2 Proteins), MMP9 (show MMP9 Proteins) and TNFalpha (show TNF Proteins) secretion of NA SMCs. In conclusion, TIMP3 may be considered a potential therapeutic drug for use in a novel drugeluting stent, to attenuate the progressive dilation of the aortic NA.
Circulating smoke components, including acrolein, contribute to vascular diseases through enhanced MMP-1 (show MMP1 Proteins) and decreased TIMP-3 secretion.
TIMP-3 is downregulated in a distinct subpopulation of atherosclerotic foam cells which have increased MMP-14 (show MMP14 Proteins).
Reactive oxygen species mediate TGF-beta1 (show TGFB1 Proteins)-induced TIMP-3 gene expression
TIMP3 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.
TIMP3 mRNA expression level was upregulated by multidirectional articular motion.
only the N-terminal, but not the C-terminal domain of TIMP-3, results in developmental defects.
metamorphic tail and intestine RNA levels of TIMP-2 (show TIMP2 Proteins), MT1-MMP (show MMP14 Proteins) and Gel-A, but not MT3-MMP (show MMP24 Proteins) or TIMP-3, are elevated during periods of cell death and proliferation
Loss of TIMP3 is associated with germinal matrix hemorrhage-intraventricular hemorrhage.
altered cortical and trabecular bone mineralization and increased compositional heterogeneity were found in Timp-3 (-/-) bone, all being indicative of high bone remodeling
In a clinically relevant CADASIL (show NOTCH3 Proteins) mouse model, we show that exogenous ADAM17 (show ADAM17 Proteins) or HB-EGF (show HBEGF Proteins) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Proteins) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3-induced deficits.
TIMP3 promotes normal microvascular endothelial cell barrier function, at least partially, through inhibition of metalloproteinase-dependent disruption of adherens junctions, and septic downregulation of TIMP3 may contribute to septic MVEC barrier dysfunction.
data strongly suggest that TIMP3 has direct neuroprotective effects that can mitigate the deleterious effects associated with TBI, an area with few if any therapeutic options.
Elevated levels of TIMP3 and vitronectin, acting downstream of Notch3(ECD) deposition, play a role in CADASIL, producing divergent influences on early CBF deficits and later white matter lesions.
4-Hydroxyisoleucine improved insulin (show INS Proteins) resistant-like state in 3T3-L1 adipocytes by targeting TACE (show ADAM17 Proteins)/TIMP3 and the insulin (show INS Proteins) signaling pathway.
In a mouse model of prostate cancer, increased tumor growth, proliferation index, increased microvascular density, and invasion was observed in Pten(-/-), Timp3(-/-) prostate tumors compared to Pten(-/-), Timp3(+/+) tumors.
Timp3 status determines p53 (show TP53 Proteins), p38 (show CRK Proteins) and Notch (show NOTCH1 Proteins) coactivation to instruct hepatic cell fate and transformation.
TIMP2 (show TIMP2 Proteins) and TIMP3 play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function
These results suggest the crucial role of TIMP-3 in successful implantation and embryo survival and indicate the endometrial stromal decidualization-like in pigs.
This gene belongs to the TIMP gene family. The proteins encoded by this gene family are inhibitors of the matrix metalloproteinases, a group of peptidases involved in degradation of the extracellular matrix (ECM). Expression of this gene is induced in response to mitogenic stimulation and this netrin domain-containing protein is localized to the ECM. Mutations in this gene have been associated with the autosomal dominant disorder Sorsby's fundus dystrophy.
metalloproteinase inhibitor 3
, TIMP metallopeptidase inhibitor 3 (Sorsby fundus dystrophy, pseudoinflammatory)
, tissue inhibitor metalloproteinase-3
, TIMP metallopeptidase inhibitor 3
, Metalloproteinase inhibitor 3
, MIG-5 protein
, protein MIG-5
, tissue inhibitor of metalloproteinases 3
, tissue inhibitor of metalloproteinase-3
, tissue inhibitor of metalloproteinase 3 (Sorsby fundus dystrophy, pseudoinflammatory)
, tissue inhibitor of metalloproteinase 3
, 21 kDa protein of extracellular matrix
, tissue inhibitor of metalloproteinases-3