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TIMP3 belongs to the TIMP gene family. Zusätzlich bieten wir Ihnen TIMP3 Antikörper (215) und TIMP3 Kits (98) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 17 products:
miR (zeige MLXIP Proteine)-21-5p mediates apoptosis by targeting PTEN and TIMP3.
Preliminary studies indicate that baseline MMP3 (zeige MMP3 Proteine) and TIMP3 concentrations are associated with patient survival and disease-free time
TIMP-3 mRNA expression levels positively correlates with levels of miR (zeige MLXIP Proteine)-21 in in situ breast carcinomas and negatively in progesterone receptor (zeige PGR Proteine) positive invasive breast carcinomas.
Sphingosine-1-phosphate inhibited cell migration and MMP-2 (zeige MMP2 Proteine) 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 (zeige CLU Proteine) 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 (zeige RECK Proteine) by downregulating microRNA-205 through regulation of the Rprd2-Dgcr8 (zeige DGCR8 Proteine)/Ddx5 (zeige DDX5 Proteine)-Dicer1 (zeige DICER1 Proteine) biogenesis pathway.
MMP-13 (zeige MMP13 Proteine) may play a role on physiological turnover of cartilage extracellular matrix and that LRP1 (zeige LRP1 Proteine) is a key modulator of extracellular levels of MMP-13 (zeige MMP13 Proteine) and its internalization is independent of the levels of ADAMTS-4 (zeige ADAMTS4 Proteine), -5 and TIMP-3.
Long noncoding RNA DANCR promotes prostate cancer invasion and metastasis through repressing the expression of TIMP2 (zeige TIMP2 Proteine)/3
we show that KDM1A (zeige KDM1A Proteine) promotes cancer metastasis in non-small cell lung cancer cells by repressing TIMP3 (tissue inhibitor of metalloproteinase 3) expression.
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 (zeige MMP2 Proteine), MMP9 (zeige MMP9 Proteine) and TNFalpha (zeige TNF Proteine) 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 (zeige MMP1 Proteine) and decreased TIMP-3 secretion.
TIMP-3 is downregulated in a distinct subpopulation of atherosclerotic foam cells which have increased MMP-14 (zeige MMP14 Proteine).
Reactive oxygen species mediate TGF-beta1 (zeige TGFB1 Proteine)-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 (zeige TIMP2 Proteine), MT1-MMP (zeige MMP14 Proteine) and Gel-A, but not MT3-MMP (zeige MMP24 Proteine) 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 (zeige NOTCH3 Proteine) mouse model, we show that exogenous ADAM17 (zeige ADAM17 Proteine) or HB-EGF (zeige HBEGF Proteine) restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (zeige KCNAB2 Proteine) (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 (zeige INS Proteine) resistant-like state in 3T3-L1 adipocytes by targeting TACE (zeige ADAM17 Proteine)/TIMP3 and the insulin (zeige INS Proteine) 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 (zeige TP53 Proteine), p38 (zeige CRK Proteine) and Notch (zeige NOTCH1 Proteine) coactivation to instruct hepatic cell fate and transformation.
TIMP2 (zeige TIMP2 Proteine) 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