anti-ADAM Metallopeptidase Domain 15 (ADAM15) Antibodies

Rabbit ADAM Metallopeptidase Domain 15 (ADAM15) interaction partners

1. ADAM15 attenuates the progression of atherosclerosis; in contrast, a mutated form of ADAM15, created by ablation of the protease function, has no significant effect on atherosclerosis.

Mouse (Murine) ADAM Metallopeptidase Domain 15 (ADAM15) interaction partners

1. findings indicated that silencing ADAM15 had antiinflammatory effects in FLSs and efficiently inhibited the development of CIA.

2. the catalytic activity of ADAM15 is not crucial for its function in promoting pathological neovascularization in the mouse OIR model, most likely because of the very limited substrate repertoire of ADAM15.

3. ADAM15 upregulation contributes to inflammatory lung injury by promoting endothelial hyperpermeability and neutrophil transmigration.

4. A disintegrin and metalloproteinase 15 contributes to atherosclerosis by mediating endothelial barrier dysfunction via Src family kinase activity.

5. Adult Adam15(-/-) mice displayed an increase in bone volume and thickness with an increase in the number and activity of osteoblasts, whereas osteoclasts were apparently unaffected.

6. ADAM15 has a role in pathological neovascularization in mice

7. cytoplasmic domain of ADAM15v2 strongly interacts with Lck and plays an important role in T lymphocytes

8. The accelerated development of murine osteoarthritis in ADAM15 deficiency and the proadhesive and cell survival-promoting in vitro effect of ADAM15 overexpression suggest a homeostatic role of ADAM15 in cartilage remodeling.

9. observations suggest that a disintegrin and metalloproteinase (ADAM)-8,-9,-10,-12,-15,and -17 play an important role in mouse uterine tissue remodelling during the oestrous cycle

10. found modest expression of ADAM15 in pericytes in normal retina and strong up-regulation of ADAM15 in retinal vascular endothelial cells in ischemic retina

11. ADAM10 performs a dual role in cells, as a metalloprotease when it is membrane-bound, and as a potential signaling protein once cleaved by ADAM9/15 and the gamma-Secretase

Human ADAM Metallopeptidase Domain 15 (ADAM15) interaction partners

1. ET-1 expression in the endothelial cells of diabetic foot ulcers is an important determinant of insulin resistance at the onset of disease and induces macrophages to produce NF-kappaB, which regulates inflammation. It is thought that ADAM 15 contributes to angiogenic effects as a means of stimulating endothelial cells

2. The results of our study demonstrate that ADAM15 is strongly up regulated in a small but highly aggressive fraction of prostate cancers.

3. Data show that ADAM9 silencing affected MMP2 and ADAM15 expression.

4. ADAM15 promotes lung cancer cell invasion through directly targeting MMP9 activation.

5. the results revealed an undescribed role of ADAM15 in the invasion of human bladder cancer and suggested that the ADAM15 catalytic domain may represent a viable therapeutic target in patients with advanced disease.

6. present a tumor suppressive mechanism for ADAM15 exosomes and provide insight into the functional significance of exosomes that generate tumor-inhibitory factors

7. these data suggest the potential role of miR147b in regulating endothelial barrier function by targeting ADAM15 expression.

8. findings indicated that silencing ADAM15 had antiinflammatory effects in FLSs and efficiently inhibited the development of CIA.

9. The severity of intrauterine adhesions positively correlates to the protein and transcript expression levels of ADAM-15 and ADAM-17 in uterine tissue.

10. ADAM15 contributes to apoptosis resistance in rheumatoid arthritis synovial fibroblasts by activating the Src/FAK pathway upon FasL exposure.

11. In conclusion, our data identified rhddADAM15 as a potent inhibitor of tumor growth and metastasis, making it a promising tool for use in anticancer treatment.

12. ADAM15 acts as a negative regulator of TRIF-mediated NF-kappaB and IFN-beta reporter gene activity via TLR3 and TLR4 signaling.

13. dispensable for cutaneous wound healing and B16F1 melanoma growth, but significantly contributes to metastasis formation

14. Exosomes rich in ADAM15 display enhanced binding affinity for integrin alphavbeta3 in an RGD-dependent manner and suppress vitronectin- and fibronectin-induced cell adhesion, growth, and migration, as well as in vivo tumor growth.

15. ADAM15 tail can transduce a percepted extracellular signal to enhance FAK and Src phosphorylation.

16. Promoter methylation of ADAM15 was examined as well as the microsatellite instability status. Thirty-six percent of colorectal carcinomas displayed a reduced expression of ADAM15.

17. gene expressions for ADAM8 and ADAM15 were notably lower in ascending aorta as compared with aortic dissection

18. demonstrate the intrinsic promoter activity of ADAM15 in quiescent mesangial cells and show the involvement of Sp1 in its regulation

19. the downregulation of ADAM15 plays an important role in melanoma progression and ADAM15 act as a tumorsuppressor in melanoma.

20. The effects of ADAM15 on endothelial hyperpermeability and neutrophil transmigration are mediated by intracellular signalling involving Src and ERK1/2 activation.