anti-ADAM Metallopeptidase with thrombospondin Type 1 Motif, 9 (ADAMTS9) Antikörper

Mouse (Murine) ADAM Metallopeptidase with thrombospondin Type 1 Motif, 9 (ADAMTS9) Interaktionspartner

1. Extracellular matrix dynamics is a major influence on umbilical vascular SMC fate, with ADAMTS9 acting as its principal mediator.

2. The present study reveals ADAMT-9 expression by mast cells(MCs) and that MC activation regulates the expression of the protease, thus implicating the ADAMT-9 of protease in MC function.

3. Western blot analyses indicated that aggrecanase-generated proteoglycan fragments are produced after SCI.

4. These findings support a model in which cooperative versican proteolysis by ADAMTS9 in vascular endothelium and by ADAMTS20 in palate mesenchyme drives palatal shelf sculpting and extension.

5. These data identify ADAMTS9 as a novel, constitutive, endogenous angiogenesis inhibitor that operates cell-autonomously in endothelial cells.

6. ancillary domains of ADAMTS-9 are required both for specific extracellular localization and for its versicanase and aggrecanase activities

7. Adamts9 is widely expressed during mouse embryo development

8. show that combinatorial mouse alleles for the secreted metalloproteases Adamts5, Adamts20 (bt), and Adamts9 result in fully penetrant soft-tissue syndactyly.

Human ADAM Metallopeptidase with thrombospondin Type 1 Motif, 9 (ADAMTS9) Interaktionspartner

1. ADAMTS9 gene cytosine-adenine repeat polymorphism may be used to determine the prognosis for knee osteoarthritis radiologic progression.

2. expression by synovial cells induced by hemoglobin at low doses, suggesting a possible role for hemoglobin in cartilage damage after intra-articular hemorrhage

3. By inhibiting ADAMTS-9, miR-338-5p suppressed the proliferation and metastasis of rheumatoid arthritis synovial fibroblasts.

4. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis.

5. Our data showed that four SNPs (rs73832338, rs9985304, rs4317088, and rs9831846) in the ADAMTS9 gene were significantly associated with cognitive aging among the subjects. Additionally, we found that interactions between the ADAMTS9 rs9985304 and ADAMTS9 rs76346246 SNPs influenced cognitive aging.

6. we identified the top 10 highly differentiated SNPs in Brazilian Amerindian ancestry compared to Asian, European, and African Genomes.SNPs within or proximal to CIITA (rs6498115), SMC6 (rs1834619), and KLHL29 (rs2288697) were most differentiated in the Amerindian-specific branch. SNPs in ADAMTS9 (rs7631391), DOCK2 (rs77594147), SLC28A1 (rs28649017), ARHGAP5 (rs7151991), and CIITA (rs45601437) in the Asian comparison.

7. study identified a suggestive genome-wide significant association of ADAMTS9 with asthma in Spanish subjects

8. NF-kappaBp65 bound to elements located at -1177 and -1335 in the ADAMTS9 promoter region, in contrast to the untreated samples. The results of the present study suggested that NF-kappaB may be involved in IL-1beta-induced activation of ADAMTS9 in human chondrocytes

9. A deletion at ADAMTS9-MAGI1 locus is associated with psoriatic arthritis risk.

10. LncRNA ADAMTS9-AS2 is regulated by DNMT1 and inhibits migration of glioma cells.

11. The present study reveals ADAMT-9 expression by mast cells(MCs) and that MC activation regulates the expression of the protease, thus implicating the ADAMT-9 of protease in MC function.

12. The pathways MAPK and NF-kappaB were responsible pathways for the induction of ADAMTS9 gene.

13. PPARG2 and ADAMTS9 variants are both associated with type 2 diabetes mellitus and with insulin resistance, whereas only ADAMTS9 may be related to beta cell function.

14. ADAMTS9 acts as a functional tumor suppressor in gastric cancer through inhibiting oncogenic AKT/mTOR signaling pathway

15. ADAMTS9 and GON-1 in the ER that promotes protein transport from the ER to the Golgi. This function is GON-domain dependent but protease activity independent.

16. Data show that the expression of ADAMTS4, 9, 16 and was up-regulated during chondrogenesis, ADAMTS1 and 5 were down-regulated.

17. four of the six aggrecanases are expressed in immortalized chondrocyte cell-lines and can be upregulated in response to inflammatory cytokines

18. Results indicate that ADAMTS9 contributes an important function in the tumor microenvironment that acts to inhibit angiogenesis and tumor growth in both esophageal cancer and nasophageal cancer.

19. These data identify ADAMTS9 as a novel, constitutive, endogenous angiogenesis inhibitor that operates cell-autonomously in endothelial cells.

20. These data identify for the first time the cellular chaperones associated with secretion of an ADAMTS protease and suggest a role for gp96 in modulating pro-ADAMTS9 processing.