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

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

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 (Montrer TNF Protéines) 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 (Montrer SLC13A2 Protéines) domain

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

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

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

2. 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.

3. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP (Montrer COMP Protéines) are associated with human AA.

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

5. miR (Montrer MLXIP Protéines)-105/Runx2 (Montrer RUNX2 Protéines) axis mediates FGF2 (Montrer FGF2 Protéines)-induced ADAMTS (Montrer ADAMTS13 Protéines) expression in osteoarthritis cartilage.

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

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

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

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

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