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

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

1. Adamts7-/- Adamts12-/- mice, but not corresponding single-gene mutants, develop progressive heterotopic ossification (HO) in tendons with abnormal collagen fibrils, accompanied by reduced levels of the small leucine-rich proteoglycans which regulate collagen fibrillogenesis. These results suggest that Adamts7 and Adamts12 drive an innate pathway protective against hindlimb HO in mice.

2. presents the expression levels of ADAMTS-7 and COMP in the decidual tissues of mice and humans suffering from SA.

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

4. 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.

5. 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.

6. The overexpression of ADATMTS-7 might contribute to early inflammatory kidney damage associated with aging

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

8. 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 domain

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

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

1. Degenerated human biceps tendons had reduced ADAMTS7 mRNA compared with healthy biceps tendons, which expressed both ADAMTS7 and ADAMTS12. These results suggest that ADAMTS7 and ADAMTS12 may be essential for human tendon health.

2. ADAMTS7 polymorphisms of both rs7173743 and rs3825807 were associated with carotid plaque vulnerability but not the prevalence of ischemic stroke. The T/T genotype of rs7173743 and A/A genotype of rs3825807 were considered as risk genotypes for vulnerable plaque susceptibility. In conclusion, ADAMTS7 variants rs3825807 and rs7173743 are associated with the risk for carotid plaque vulnerability.

3. Serum ADAMTS7 level is positively associated with acute coronary syndrome, and patients with the CT/TT genotype at the rs1994016 allele are less prone to suffer from ACS.

4. presents the expression levels of ADAMTS-7 and COMP in the decidual tissues of mice and humans suffering from SA.

5. data show that ADAMTS-7 is associated with a vulnerable plaque phenotype in human carotid lesions. These data support previous observations of a potential proatherogenic role of ADAMTS-7.

6. Multivariate analysis showed that DeltaADAMTS-7(day 7 minus day 1) was independently associated with left ventricular reverse remodeling

7. Genetic variation at the ADAMTS7 locus is associated with reduced severity of coronary artery disease.

8. 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.

9. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP are associated with human AA.

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

11. miR-105/Runx2 axis mediates FGF2-induced ADAMTS expression in osteoarthritis cartilage.

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

13. During inflammatory conditions, AP-1 and Sp1 sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells

14. ADAMTS7 and LPA single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.

15. Expression of miR-26a and miR-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, COL4A2, CPEB3, CDK6, DNMT3a and PI3KR1 was significantly down regulated in at least two of three disease types with respect to normal tissues.

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

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

18. The significant associations observed between this coding variant in ADAMTS7 and the risk of CAD development.

19. Logistic regression analysis indicated that the association between ADAMTS-7 and heart failure after AMI was independent from traditional cardiovascular risk factors and other biomarkers

20. Data conclude that ADAMTS-7 level appears to be positively associated with expression of TNF-alpha and Phospho-NF-kappaB P65 in cartilage, which may imply its association with cartilage destruction of ONFH.