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TIMP3 belongs to the TIMP gene family. Zusätzlich bieten wir Ihnen TIMP3 Kits (106) und TIMP3 Proteine (20) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal TIMP3 Primary Antibody für IF (p), IHC (p) - ABIN668361
Liu, Cui, Ao, Zhou, Zhou, Yuan, Xiang, Liu, Cao et al.: Aberrant methylation accounts for cell adhesion-related gene silencing during 3-methylcholanthrene and diethylnitrosamine induced multistep rat lung carcinogenesis associated with overexpression of ... in Toxicology and applied pharmacology 2011
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Human Polyclonal TIMP3 Primary Antibody für EIA, FACS - ABIN955222
Wick, Härönen, Mumberg, Bürger, Olsen, Budarf, Apte, Müller: Structure of the human TIMP-3 gene and its cell cycle-regulated promoter. in The Biochemical journal 1995
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Human Polyclonal TIMP3 Primary Antibody für IHC, ELISA - ABIN1585860
Nakasone, Terasako-Saito, Yamazaki, Sato, Tanaka, Sakamoto, Kurita, Yamasaki, Wada, Ishihara, Kawamura, Machishima, Ashizawa, Kimura, Kikuchi, Tanihara, Kanda, Kako, Nishida, Yamada, Kanda: Impact of high-/middle-molecular-weight adiponectin on the synthesis and regulation of extracellular matrix in dermal fibroblasts. in Experimental hematology 2014
Human Monoclonal TIMP3 Primary Antibody für FACS - ABIN4896675
Mahller, Vaikunth, Ripberger, Baird, Saeki, Cancelas, Crombleholme, Cripe: Tissue inhibitor of metalloproteinase-3 via oncolytic herpesvirus inhibits tumor growth and vascular progenitors. in Cancer research 2008
Human Polyclonal TIMP3 Primary Antibody für ELISA, WB - ABIN1533421
Silbiger, Jacobsen, Cupples, Koski: Cloning of cDNAs encoding human TIMP-3, a novel member of the tissue inhibitor of metalloproteinase family. in Gene 1994
Electrostatic potential calculations suggested a competition between negatively charged GAGs and highly negatively charged complement-like domains of LRP-1 (zeige LRP1 Antikörper) 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 Antikörper) Metabolic Pathway Are Associated with Lumbar Disc Degeneration and Modic Changes
Our data suggest that miR (zeige MLXIP Antikörper)-206 may function as an inflammatory regulator and drive the expression of MMP9 (zeige MMP9 Antikörper) in M.tb-infected THP-1 (zeige GLI2 Antikörper) cells by targeting TIMP3, indicating that miR (zeige MLXIP Antikörper)-206 is a potential therapeutic target for patients with TB.
Plasma TIMP3 is a biomarker for predicting the tumor stage in patients with oral squamous cell carcinoma .
TIMP-3 K26A/K45A retained higher affinity for sulfated (zeige SULF1 Antikörper) glycosaminoglycans than K42A/K110A and exhibited increased affinity for ADAMTS-5 (zeige ADAMTS5 Antikörper) in the presence of heparin.
Of the 225 genetic tests performed, 150 were for recessive IRD (zeige SCRIB Antikörper), and 75 were for dominant IRD (zeige SCRIB Antikörper). A positive molecular diagnosis was made in 70 (59%) of probands with recessive IRD (zeige SCRIB Antikörper) and 19 (26%) probands with dominant IRD (zeige SCRIB Antikörper). Thirty-two novel variants were identified; among these, 17 sequence changes in four genes were predicted to be possibly or probably damaging including: ABCA4 (zeige ABCA4 Antikörper) (14), BEST1 (zeige BEST1 Antikörper) (2), PRPH2 (zeige PRPH2 Antikörper) (1), and TIMP3
Study evaluated MMP-12 (zeige MMP12 Antikörper) and TIMP-1 (zeige TIMP1 Antikörper), TIMP-2 (zeige TIMP2 Antikörper), TIMP-3, and TIMP-4 (zeige TIMP4 Antikörper) levels in 40 patients with asymptomatic and symptomatic critical carotid artery stenosis (CAS (zeige CSE1L Antikörper)) with neurologic symptoms onset within the preceding 12 hours; results suggest that MMP-12 (zeige MMP12 Antikörper) is related to critical CAS (zeige CSE1L Antikörper) independently on symptoms, moreover, TIMP-3 and TIMP-4 (zeige TIMP4 Antikörper) seem to be specifically related to stroke
A total of 1096 subjects from eight studies were included in the present meta-analysis. Overall, a significant association between TIMP-3 methylation and gastric cancer risk was observed (OR = 8.65; 95% CI4.31-17.37; p < 0.001). Our results show a positive correlation between TIMP-3 promoter methylation and gastric cancer risk and that TIMP-3 promoter methylation may be used as a molecular marker for gastric cancer
TIMP-3 expression is suppressed by promoter methylation in HCC (zeige FAM126A Antikörper).
Circulating smoke components, including acrolein, contribute to vascular diseases through enhanced MMP-1 (zeige MMP1 Antikörper) and decreased TIMP-3 secretion.
TIMP-3 is downregulated in a distinct subpopulation of atherosclerotic foam cells which have increased MMP-14 (zeige MMP14 Antikörper).
Reactive oxygen species mediate TGF-beta1 (zeige TGFB1 Antikörper)-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 Antikörper), MT1-MMP (zeige MMP14 Antikörper) and Gel-A, but not MT3-MMP (zeige MMP24 Antikörper) or TIMP-3, are elevated during periods of cell death and proliferation
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 (zeige VTN Antikörper), acting downstream of Notch3 (zeige NOTCH3 Antikörper)(ECD (zeige ECD Antikörper)) deposition, play a role in CADASIL (zeige NOTCH3 Antikörper), producing divergent influences on early CBF (zeige CEBPZ Antikörper) deficits and later white matter lesions.
4-Hydroxyisoleucine improved insulin (zeige INS Antikörper) resistant-like state in 3T3-L1 adipocytes by targeting TACE (zeige ADAM17 Antikörper)/TIMP3 and the insulin (zeige INS Antikörper) signaling pathway.
In a mouse model of prostate cancer, increased tumor growth, proliferation index, increased microvascular density, and invasion was observed in Pten (zeige PTEN Antikörper)(-/-), Timp3(-/-) prostate tumors compared to Pten (zeige PTEN Antikörper)(-/-), Timp3(+/+) tumors.
Timp3 status determines p53 (zeige TP53 Antikörper), p38 (zeige CRK Antikörper) and Notch (zeige NOTCH1 Antikörper) coactivation to instruct hepatic cell fate and transformation.
TIMP2 (zeige TIMP2 Antikörper) 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 Antikörper)/Timp3-deficient mice.
lack of TIMP3 increases inflammation and polarizes macrophages towards a more inflammatory phenotype resulting in increased atherosclerosis.
TIMP-3 KO mice exhibit enhanced metabolism, as reflected by a higher body temperature than WT mice, possibly due to increased mitochondrial activity.
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