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TIMP3 belongs to the TIMP gene family. Zusätzlich bieten wir Ihnen TIMP3 Antikörper (191) und TIMP3 Kits (106) und viele weitere Produktgruppen zu diesem Protein an.
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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.
Dissecting the interaction between TIMP3 and LRP1 (zeige LRP1 Proteine) using a synthetic analog of the LRP1 (zeige LRP1 Proteine) receptor has been reported.
These results implicate TIMP3 as a modulator of cell surface GHR (zeige GHR Proteine) abundance and the ability of GH to promote cellular signaling.
native glycosaminoglycans interact with TIMP-3.
The expression level of LIPC (zeige LIPC Proteine), SLC16A8, and TIMP-3 was significantly associated with age-related macular degeneration pathology.
Levels of miR (zeige MLXIP Proteine)-221/222 are associated negatively with estrogen receptor (zeige ESR1 Proteine) in in situ tumors and positively with tissue inhibitor of metalloproteinase 3 TIMP3 messenger RNA expression levels in pure invasive breast cancers.
Electrostatic potential calculations suggested a competition between negatively charged GAGs and highly negatively charged complement-like domains of LRP-1 (zeige LRP1 Proteine) for the binding to a positively charged area of TIMP-3 as an underlying mechanism.
TIMP3 overexpression after myocardial infarction improves myocardial structural remodeling and function by promoting angiogenesis and inhibiting early proteolysis.
Single Nucleotide Variants of Candidate Genes in Aggrecan (zeige ACAN Proteine) Metabolic Pathway Are Associated with Lumbar Disc Degeneration and Modic Changes
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
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
Expansion of stem cells counteracts age-related mammary regression in compound Timp1 (zeige TIMP1 Proteine)/Timp3-deficient mice.
lack of TIMP3 increases inflammation and polarizes macrophages towards a more inflammatory phenotype resulting in increased atherosclerosis.
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