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TIMP3 belongs to the TIMP gene family. Additionally we are shipping TIMP3 Kits (76) and TIMP3 Proteins (18) and many more products for this protein.
Showing 10 out of 186 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 3 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 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
expression of TIMP3 is low in pituitary adenomas including ACTH (show POMC Antibodies)-secreting pituitary adenomas and negatively associated with tumor aggressiveness.
Genotypes of rs135025 and rs80272 in TIMP3 contribute to the development of preeclampsia in Han Chinese women.
TIMP3 was validated as a direct target of miRNA-21 by dual-luciferase reporter assay. Silencing with small interfering RNA against TIMP3 promoted angiogenesis and increased MMP2 (show MMP2 Antibodies) and MMP9 (show MMP9 Antibodies) expression at the protein level.
TIMP3 is a dominant negative regulator of angiogenesis in cutaneous melanoma and gene silencing by promoter methylation is associated with poor outcome
Taken together, our results suggest that the imbalance between aggrecanase (show ADAMTS4 Antibodies) and TIMP-3 may play an important role in the pathogenesis of IDD (show COL9A3 Antibodies) and therefore be a potential therapeutic target for treating IDD (show COL9A3 Antibodies).
Gene-gene interactions between Smad3 (show SMAD3 Antibodies) rs6494629T/C and TIMP3 rs715572G/A polymorphisms may play more important protective roles in knee OA.
Results suggest that gene-environment interactions between the TIMP3 rs9862 polymorphisms and betel quid may alter oral cancer susceptibility and tumor growth in Taiwanese men.
following acute ACL (show ACLY Antibodies) injury, an upregulation of TIMP-3, the primary aggrecanase (show ADAMTS4 Antibodies) inhibitor, is elicited in response to increased aggrecan (show ACAN Antibodies) degradation, which may inhibit further cleavage
TIMP3) promotes endothelial apoptosis via a caspase (show CASP3 Antibodies)-independent mechanism.
This data shows that increased expression of miR (show MLXIP Antibodies)-21 enhanced the invasive potential of melanoma cell lines through TIMP3 inhibition.
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