TIMP Metallopeptidase Inhibitor 3 (TIMP3) ELISA Kits

Human TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. the present study demonstrated the regulatory contribution of SNHG16/miR-17-5p/TIMP3 axis to viability, apoptosis, proliferation, and epithelial-mesenchymal transition of bladder cancer cells, which directly affected tumor progression.

2. The presence of CpG islands hemimethylation in tissue inhibitor of metalloproteinases 3 and O-6-methylguanine-DNA methyltransferase genes is a promising triage method in cervical intraepithelial neoplasia recurrence.

3. This study demonstrated that miR-191 promoted the cell growth and invasion ability in prostate cancer through downregulating TIMP3 and might be a potential target for the biotherapy for Prostate cancer (PCa).

4. our results suggest that TIMP3 reversely mediates UVR-induced inflammation by being highly expressed during the daytime; therefore, recovering the circadian expression of TIMP3 using synthetic TIMP3 peptides or bioactive natural ingredients could at least in part inhibit the UVR-induced cellular phenomena.

5. In aortic valves, disturbed flow leads to downregulation of TIMP3 via mechanosensitive microRNA-181b and results in endothelial matrix degradation.

6. ADAMTS-2, collagen type-1, TIMP-3 and papilin levels of the uterosacral ligament play essential roles in the etiopathogenesis of pelvic organ prolapse among postmenopausal women without stress urinary incontinence.

7. The down-regulation of miR-21 inhibited the progression of diabetic nephropathy by targeting TIMP3.

8. we have shown that deleterious variation in TIMP3 is associated with bicuspid aortic valve and indices of thoracic aortic aneurysm. We further found that there is a synergistic interaction between loss of the X chromosome gene, TIMP1, and deleterious variation in TIMP3 that significantly increases that risk.

9. MiR-21 was up-regulated in cervical cancer tissues and serum samples, in contrast, TIMP3 was down-regulated in cervical cancer tissues. MiR-21 promoted the proliferation, viability and the migratory and invasive activities of cervical cancer cells through targeting TIMP3. Overexpression of TIMP3 attenuated the positive effects of miR-21.

10. Both combinations were able to increase the expressions of p53, TIMP-3 proteins, and MiR-34a in the HeLa cells.

11. these results demonstrate that decreased TIMP-3 expression may contribute to cisplatin resistance via inhibition of mitochondria-dependent apoptosis, indicating that forced TIMP-3 expression may be a useful strategy to improve the efficacy of cisplatin to treat laryngeal carcinoma

12. Genetic variation in the TIMP-3 gene may contribute to individual differences in mixture plaque susceptibility in the Han Chinese population.

13. TIMP3 methylation is a marker for TN tumours and furthermore we showed for the first time that TIMP3 promoter methylation is an epigenetic marker of BRCA1ness tumours.

14. As a novel CLOCK-dependent diurnal gene, TIMP3 inhibits the expression of inflammatory cytokines that are up-regulated by UV irradiation in human keratinocytes.

15. miR-21-5p mediates apoptosis by targeting PTEN and TIMP3.

16. Preliminary studies indicate that baseline MMP3 and TIMP3 concentrations are associated with patient survival and disease-free time

17. TIMP-3 mRNA expression levels positively correlates with levels of miR-21 in in situ breast carcinomas and negatively in progesterone receptor positive invasive breast carcinomas.

18. Sphingosine-1-phosphate inhibited cell migration and MMP-2 expression through the upregulation of the tissue inhibitor of metalloproteinase-3 (TIMP-3) expression in human chondrosarcoma cells.

19. Using global proteomic profiling of brain leptomeningeal arteries, this study revealed that clusterin and tissue inhibitor of metalloproteinases-3 increase in leptomeningeal arteries affected by cerebral amyloid angiopathy.

20. 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.

Rabbit TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. 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, MMP9 and TNFalpha 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.

2. Circulating smoke components, including acrolein, contribute to vascular diseases through enhanced MMP-1 and decreased TIMP-3 secretion.

3. TIMP-3 is downregulated in a distinct subpopulation of atherosclerotic foam cells which have increased MMP-14.

Cow (Bovine) TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. Reactive oxygen species mediate TGF-beta1-induced TIMP-3 gene expression

2. 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.

3. TIMP3 mRNA expression level was upregulated by multidirectional articular motion.

Xenopus laevis TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. only the N-terminal, but not the C-terminal domain of TIMP-3, results in developmental defects.

2. metamorphic tail and intestine RNA levels of TIMP-2, MT1-MMP and Gel-A, but not MT3-MMP or TIMP-3, are elevated during periods of cell death and proliferation

Mouse (Murine) TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. the absence of TIMP-3 leads to a more pro-angiogenic microenvironment, playing a key role in choroidal neovascularization formation by positively modulating M2 polarization.

2. the aim of this study was to determine whether Acanthamoeba spp. may affect the levels of matrix metalloproteinases (MMP-2,-9), their tissue inhibitors (TIMP-1,-3) and MMP-9/TIMP-1, MMP-2/TIMP-3 ratios in the cerebral cortex and hippocampus, in relation to the host's immunological status.

3. The data indicate that hepatic TIMP3 expression can slow the progression of nonalcoholic fatty liver disease and tumorigenesis, at least in part, through the regulation of ADAM17 activity.

4. Loss of Timp3 enhanced the susceptibility to iron overload-mediated heart and liver injury, suggesting that Timp3 is a key protective molecule against iron-mediated pathology.

5. Loss of TIMP3 is associated with germinal matrix hemorrhage-intraventricular hemorrhage.

6. altered cortical and trabecular bone mineralization and increased compositional heterogeneity were found in Timp-3 (-/-) bone, all being indicative of high bone remodeling

7. In a clinically relevant CADASIL mouse model, we show that exogenous ADAM17 or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3-induced deficits.

8. 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.

9. 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.

10. 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.

11. 4-Hydroxyisoleucine improved insulin resistant-like state in 3T3-L1 adipocytes by targeting TACE/TIMP3 and the insulin signaling pathway.

12. 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.

13. Timp3 status determines p53, p38 and Notch coactivation to instruct hepatic cell fate and transformation.

14. TIMP2 and TIMP3 play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function

15. Expansion of stem cells counteracts age-related mammary regression in compound Timp1/Timp3-deficient mice.

16. lack of TIMP3 increases inflammation and polarizes macrophages towards a more inflammatory phenotype resulting in increased atherosclerosis.

17. TIMP-3 KO mice exhibit enhanced metabolism, as reflected by a higher body temperature than WT mice, possibly due to increased mitochondrial activity.

18. TIMP3 protects kidney from damage

19. TIMP3 reduction is due, at least in part, to increased expression of certain TIMP3-targeting microRNAs in diabetic kidneys compared to healthy controls.

20. Demonstrate a critical role for TIMP3, among all TIMPs, in preserving arterial remodelling in response to Ang II-induced hypertension.

Pig (Porcine) TIMP Metallopeptidase Inhibitor 3 (TIMP3) Interaktionspartner

1. miR-21 promotes cumulus expansion and oocyte maturation via down-regulating TIMP3

2. These results suggest the crucial role of TIMP-3 in successful implantation and embryo survival and indicate the endometrial stromal decidualization-like in pigs.