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The protein encoded by ADAMTS7 is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family. De plus, nous expédions ADAMTS7 Kits (23) et ADAMTS7 Protéines (9) et beaucoup plus de produits pour cette protéine.
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Therefore, these data provided the in vivo evidence, suggesting that ADAMTS-7 may play an important role in the pathogenesis of inflammatory arthritis.
Mice lacking Adamts7, Ldlr, Apoe had less lesion formation in aortas and aortic roots vs controls and less neointimal formation after femoral wire injury. Adamts7 expression was induced by injury and hyperlipidemia.
Adamts-7 deficiency substantially ameliorated neointima formation in mice at days 14 and 28 after injury. ADAMTS-7 inhibited both endothelial cell proliferation and migration.
ADAMTS-7 and TNF-alpha (Montrer TNF Anticorps) form a positive feedback loop in the regulation of cartilage degradation and osteoarthritis progression.
ADAMTS7B has a domain organization with a total of eight thrombospondin type 1 repeats in its ancillary domain. Of these, seven are arranged in two distinct clusters that are separated by a mucin (Montrer SLC13A2 Anticorps) domain
Findings demonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone formation by associating with and inactivating GEP (Montrer GRN Anticorps) chondrogenic growth factor.
The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP (Montrer COMP Anticorps) are associated with human AA.
The native overfunctional ADAMTS7 allele (A) may accelerate VSMC migration and lead to neointimal thickening, atherosclerosis progression and acute plaque events.
miR (Montrer MLXIP Anticorps)-105/Runx2 (Montrer RUNX2 Anticorps) axis mediates FGF2 (Montrer FGF2 Anticorps)-induced ADAMTS (Montrer ADAMTS13 Anticorps) expression in osteoarthritis cartilage.
Allelic variation that associates with reduced ADAMTS7 expression confers stronger coronary heart disease protection in never-smokers than in ever-smokers.
During inflammatory conditions, AP-1 (Montrer FOSB Anticorps) and Sp1 (Montrer PSG1 Anticorps) sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells
ADAMTS7 and LPA (Montrer APOA Anticorps) single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.
Expression of miR (Montrer MLXIP Anticorps)-26a and miR (Montrer MLXIP Anticorps)-29a was significantly down regulated in leukoplakia and cancer tissues but up regulated in lichen planus tissues. Expression of target genes such as, ADAMTS7, ATP1B1 (Montrer ATP1B1 Anticorps), COL4A2 (Montrer COL4a2 Anticorps), CPEB3 (Montrer CPEB3 Anticorps), CDK6 (Montrer CDK6 Anticorps), DNMT3a (Montrer DNMT3A Anticorps) and PI3KR1 was significantly down regulated in at least two of three disease types with respect to normal tissues.
Our results indicate the presence of ADAMTS-7 in human NP cells and imply its potential role in disc degeneration.
The main contribution of this study is the proposal of a pharmacophore for ADAMTS7.
The significant associations observed between this coding variant in ADAMTS7 and the risk of CAD (Montrer CAD Anticorps) development.
The protein encoded by this gene is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family. Members of this family share several distinct protein modules, including a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and a thrombospondin type 1 (TS) motif. Individual members of this family differ in the number of C-terminal TS motifs, and some have unique C-terminal domains. The protein encoded by this gene contains two C-terminal TS motifs.
ADAM metallopeptidase with thrombospondin type 1 motif, 7
, A disintegrin and metalloproteinase with thrombospondin motifs 7
, ADAM-TS 7
, a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 7
, a disintegrin and metalloprotease with thrombospondin motifs-7 preproprotein
, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 7