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The protein encoded by ADAMTS7 is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family. 再加上，我们可以发ADAMTS7 试剂盒 (23) 和 ADAMTS7 蛋白 (9)和数多这个蛋白质的别的产品。
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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 (显示 TNF 抗体) 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 (显示 SLC13A2 抗体) domain
Findings demonstrate that ADAMTS-7, a direct target of PTHrP (显示 PTHLH 抗体) signaling, negatively regulates endochondral bone formation by associating with and inactivating GEP (显示 GRN 抗体) chondrogenic growth factor.
miR (显示 MLXIP 抗体)-105/Runx2 (显示 RUNX2 抗体) axis mediates FGF2 (显示 FGF2 抗体)-induced ADAMTS (显示 ADAMTS13 抗体) 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 (显示 FOSB 抗体) and Sp1 (显示 PSG1 抗体) sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells
ADAMTS7 and LPA single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.
Expression of miR (显示 MLXIP 抗体)-26a and miR (显示 MLXIP 抗体)-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 (显示 ATP1B1 抗体), COL4A2 (显示 COL4a2 抗体), CPEB3 (显示 CPEB3 抗体), CDK6 (显示 CDK6 抗体), DNMT3a (显示 DNMT3A 抗体) 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 (显示 CAD 抗体) development.
Logistic regression analysis indicated that the association between ADAMTS-7 and heart failure after AMI (显示 CFD 抗体) was independent from traditional cardiovascular risk factors and other biomarkers
Data conclude that ADAMTS-7 level appears to be positively associated with expression of TNF-alpha (显示 TNF 抗体) and Phospho-NF-kappaB (显示 NFKB1 抗体) P65 (显示 GORASP1 抗体) in cartilage, which may imply its association with cartilage destruction of ONFH.
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