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TIMP3 belongs to the TIMP gene family. Additionally we are shipping TIMP3 Kits (89) and TIMP3 Proteins (21) and many more products for this protein.
Showing 10 out of 173 products:
Human Polyclonal TIMP3 Primary Antibody for 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
Show all 5 references for ABIN668361
Human Polyclonal TIMP3 Primary Antibody for 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
Show all 2 references for ABIN955222
Human Monoclonal TIMP3 Primary Antibody for 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 for 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
Human Polyclonal TIMP3 Primary Antibody for 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
Of the 225 genetic tests performed, 150 were for recessive IRD (show SCRIB Antibodies), and 75 were for dominant IRD (show SCRIB Antibodies). A positive molecular diagnosis was made in 70 (59%) of probands with recessive IRD (show SCRIB Antibodies) and 19 (26%) probands with dominant IRD (show SCRIB Antibodies). Thirty-two novel variants were identified; among these, 17 sequence changes in four genes were predicted to be possibly or probably damaging including: ABCA4 (show ABCA4 Antibodies) (14), BEST1 (show BEST1 Antibodies) (2), PRPH2 (show PRPH2 Antibodies) (1), and TIMP3
Study evaluated MMP-12 (show MMP12 Antibodies) and TIMP-1 (show TIMP1 Antibodies), TIMP-2 (show TIMP2 Antibodies), TIMP-3, and TIMP-4 (show TIMP4 Antibodies) levels in 40 patients with asymptomatic and symptomatic critical carotid artery stenosis (CAS (show CSE1L Antibodies)) with neurologic symptoms onset within the preceding 12 hours; results suggest that MMP-12 (show MMP12 Antibodies) is related to critical CAS (show CSE1L Antibodies) independently on symptoms, moreover, TIMP-3 and TIMP-4 (show TIMP4 Antibodies) 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 (show FAM126A Antibodies).
Both TIMP3 and APC (show APC Antibodies) methylation were associated with lymph node metastasis and higher clinical stage of tumors. Patients with methylation at TIMP3 or APC (show APC Antibodies) had worse prognoses as compared to those without these alterations.
Data indicate the TGF-beta (show TGFB1 Antibodies) pathway regulates the epithelial-to-mesenchymal transition (EMT (show ITK Antibodies)) of gastric cancer cells by increasing the levels of microRNA miRNA-181b to target Timp3 via the Smad2 (show SMAD2 Antibodies)/3/4-dependent pathway.
Study identifies 2 urinary biomarkers-bFGF (show FGF2 Antibodies) and TIMP3-that successfully detect one of the most common pediatric brain tumors, juvenile pilocytic astrocytomas, with high accuracy
the levels of TIMP-3, and in some cases also TIMP-2 (show TIMP2 Antibodies), are decreased in Emery-Dreifuss muscular dystrophy (EDMD (show EMD Antibodies)). The decrease might be associated with an adverse effect on matrix metalloproteinases and remodelling of the myocardial matrix. The specific decrease of TIMP-3 indicates that this biomarker might help in early detection of cardiac involvement in EDMD (show EMD Antibodies).
TIMP3 knockdown had opposite effects on the regulation of these genes.
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 (show TIMP2 Antibodies) and TIMP3 with MMP9 (show MMP9 Antibodies) activity
Circulating smoke components, including acrolein, contribute to vascular diseases through enhanced MMP-1 (show MMP1 Antibodies) and decreased TIMP-3 secretion.
TIMP-3 is downregulated in a distinct subpopulation of atherosclerotic foam cells which have increased MMP-14 (show MMP14 Antibodies).
Reactive oxygen species mediate TGF-beta1 (show TGFB1 Antibodies)-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 Antibodies), MT1-MMP (show MMP14 Antibodies) and Gel-A, but not MT3-MMP (show MMP24 Antibodies) or TIMP-3, are elevated during periods of cell death and proliferation
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 (show VTN Antibodies), acting downstream of Notch3 (show NOTCH3 Antibodies)(ECD (show ECD Antibodies)) deposition, play a role in CADASIL (show NOTCH3 Antibodies), producing divergent influences on early CBF (show CEBPZ Antibodies) deficits and later white matter lesions.
4-Hydroxyisoleucine improved insulin (show INS Antibodies) resistant-like state in 3T3-L1 adipocytes by targeting TACE (show ADAM17 Antibodies)/TIMP3 and the insulin (show INS Antibodies) signaling pathway.
In a mouse model of prostate cancer, increased tumor growth, proliferation index, increased microvascular density, and invasion was observed in Pten (show PTEN Antibodies)(-/-), Timp3(-/-) prostate tumors compared to Pten (show PTEN Antibodies)(-/-), Timp3(+/+) tumors.
Timp3 status determines p53 (show TP53 Antibodies), p38 (show CRK Antibodies) and Notch (show NOTCH1 Antibodies) coactivation to instruct hepatic cell fate and transformation.
TIMP2 (show TIMP2 Antibodies) 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 (show TIMP1 Antibodies)/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.
TIMP3 protects kidney from damage
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