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The protein encoded by ADAMTS7 is a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family.
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Human ADAMTS7 ELISA Kit für Sandwich ELISA - ABIN415115
Serra, Gallelli, Butrico, Buffone, Caliò, De Caridi, Massara, Barbetta, Amato, Labonia, Mimmi, Iaccino, de Franciscis: From varices to venous ulceration: the story of chronic venous disease described by metalloproteinases. in International wound journal 2016
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Rat (Rattus) ADAMTS7 ELISA Kit für Sandwich ELISA - ABIN432446
Wu, Wang, Yu, Li, Gao, Ke, Wang, Zhou, Zheng: Association of ADAMTS-7 Levels with Cardiac Function in a Rat Model of Acute Myocardial Infarction. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2016
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 (zeige TNF ELISA Kits) 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 (zeige SLC13A2 ELISA Kits) domain
Findings demonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone formation by associating with and inactivating GEP (zeige GRN ELISA Kits) chondrogenic growth factor.
Studied gene expression of genetic variants of ADAMTS7 in atherosclerotic occlusive peripheral arterial disease (PAD). Found mRNA levels of ADAMTS7 to be significantly higher in PAD patients than controls, and that the rs1994016 CC and rs3825807 TT genotypes may upregulate ADAMTS7 mRNA levels and may influence PAD development.
The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP (zeige COMP ELISA Kits) 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 (zeige MLXIP ELISA Kits)-105/Runx2 (zeige RUNX2 ELISA Kits) axis mediates FGF2 (zeige FGF2 ELISA Kits)-induced ADAMTS (zeige ADAMTS13 ELISA Kits) 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 (zeige FOSB ELISA Kits) and Sp1 (zeige PSG1 ELISA Kits) sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells
ADAMTS7 and LPA (zeige APOA ELISA Kits) single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.
Expression of miR (zeige MLXIP ELISA Kits)-26a and miR (zeige MLXIP ELISA Kits)-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 (zeige ATP1B1 ELISA Kits), COL4A2 (zeige COL4a2 ELISA Kits), CPEB3, CDK6 (zeige CDK6 ELISA Kits), DNMT3a (zeige DNMT3A ELISA Kits) 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 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