anti-ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 (ADAMTS7) Antikörper

Mouse (Murine) ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 (ADAMTS7) Interaktionspartner

1. Therefore, these data provided the in vivo evidence, suggesting that ADAMTS-7 may play an important role in the pathogenesis of inflammatory arthritis.

2. 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.

3. 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.

4. ADAMTS-7 and TNF-alpha (zeige TNF Antikörper) form a positive feedback loop in the regulation of cartilage degradation and osteoarthritis progression.

5. 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 Antikörper) domain

6. Findings demonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone formation by associating with and inactivating GEP (zeige GRN Antikörper) chondrogenic growth factor.

Human ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 (ADAMTS7) Interaktionspartner

1. 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.

2. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP (zeige COMP Antikörper) are associated with human AA.

3. The native overfunctional ADAMTS7 allele (A) may accelerate VSMC migration and lead to neointimal thickening, atherosclerosis progression and acute plaque events.

4. miR (zeige MLXIP Antikörper)-105/Runx2 (zeige RUNX2 Antikörper) axis mediates FGF2 (zeige FGF2 Antikörper)-induced ADAMTS (zeige ADAMTS13 Antikörper) expression in osteoarthritis cartilage.

5. Allelic variation that associates with reduced ADAMTS7 expression confers stronger coronary heart disease protection in never-smokers than in ever-smokers.

6. During inflammatory conditions, AP-1 (zeige FOSB Antikörper) and Sp1 (zeige PSG1 Antikörper) sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells

7. ADAMTS7 and LPA (zeige APOA Antikörper) single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.

8. Expression of miR (zeige MLXIP Antikörper)-26a and miR (zeige MLXIP Antikörper)-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 Antikörper), COL4A2 (zeige COL4a2 Antikörper), CPEB3 (zeige CPEB3 Antikörper), CDK6 (zeige CDK6 Antikörper), DNMT3a (zeige DNMT3A Antikörper) and PI3KR1 was significantly down regulated in at least two of three disease types with respect to normal tissues.

9. Our results indicate the presence of ADAMTS-7 in human NP cells and imply its potential role in disc degeneration.

10. The main contribution of this study is the proposal of a pharmacophore for ADAMTS7.