Browse our anti-ADAM8 (ADAM8) Antibodies

Human ADAM Metallopeptidase Domain 8 (ADAM8) interaction partners

1. Blood ADAM 8 is a promising biomarker for early detection of gastric cancer.

2. ADAMs binds to integrins to regulate cell adhesion and migration.

3. ADAM8 is a marker of residual CML cells.

4. Authors conclude that ADAM8 promotes early metastatic processes such as transendothelial migration by upregulation of MMP-9 and shedding of PSGL-1 from breast cancer cells.

5. ADAM8 on leukocytes holds a proinflammatory function in acute lung inflammation by promoting alveolar leukocyte recruitment.

6. miR-720 is elevated in serum of patients with ADAM8-high TNBC and, in a group with other miRNAs downstream of ADAM8, holds promise as a biomarker for early detection of or treatment response of ADAM8-positive triple-negative breast cancer

7. ADAM8 causes temozolomide resistance in glioblastoma cells by enhancing pAkt/PI3K, pERK1/2, and cleavage of CD44 and HGF R/c-met

8. ADAM8 promotes GC cell proliferation and invasion, and its expression is positively correlated with poor survival, indicating that it might be a promising target in GC therapy

9. ADAM8 expression is associated with increased migration and invasiveness of pancreatic ductal adenocarcinoma cells.

10. ADAM8 and endostatin play a role in osteosarcoma progression.

11. Data indicate that fibronectin fragments (FN-fs) are present in adult ntervertebral disc (IVD) from adult subjects, and ADAM-8, known to cleave FN, is present at the pericellular matrix of disc cells.

12. Results show that ADAM8 is overexpressed in colorectal cancer and promotes cell growth.

13. N-glycosylation is essential for processing, localization, stability, and activity of ADAM8.

14. ADAM8 expression is increased in both severe asthma and COPD and associated with sputum total cell count and neutrophils. ADAM8 may facilitate neutrophil migration to the airways in severe asthma and COPD.

15. ADAM8 is abundantly expressed in breast tumors and derived metastases compared to normal tissue.

16. High ADAM8 expression is associated with pancreatic adenocarcinoma.

17. Data show that Cu2+-generated reactive oxygen species (ROS), human ADAM8, ADAM10, and ADAM17 are all capable of cleaving mouse PrP (MoPrP).

18. ADAM8 was highly expressed in 54.3% of hepatocellular carcinoma patients. ADAM8 expression was closely associated with tumor size, histological differentiation, recurrence, metastasis, and stage. High levels of ADAM8 resulted in poor prognosis.

19. We used immunohistochemistry to compare ADAM8 protein expression in HCC and normal liver tissues and further analyze the ADAM8 protein expression in 105 HCC cases. Studied knocked down expression of ADAM8 in HepG2 cells.

20. ADAM8 was robustly expressed by airway granulocytes in lung sections from human asthma patients

Mouse (Murine) ADAM Metallopeptidase Domain 8 (ADAM8) interaction partners

1. ADAMs binds to integrins to regulate cell adhesion and migration.

2. In mice, Adam8 was highly expressed in circulating neutrophils and in macrophages. Moreover, ADAM8 deficient mouse macrophages displayed reduced secretion of inflammatory mediators. Remarkably, however, neither hematopoietic nor whole-body ADAM8 deficiency in mice affected atherosclerotic lesion size.

3. Gene expression of adam8 was elevated at all time points after injury.

4. ADAM8 on leukocytes holds a proinflammatory function in acute lung inflammation by promoting alveolar leukocyte recruitment.

5. The important role of ADAM8 in the progression of hepatocellular carcinoma induced by diethylnitrosamine in mice

6. ADAM8 mediates an enhanced invasiveness of neutrophils into injured muscle fibers by the removal of their adhesiveness to blood vessels after infiltration into interstitial tissues.

7. ADAM8 has anti-inflammatory activities during allergic airway inflammation in mice

8. overexpression of PrP(C) led to up-regulation of ADAM8, suggesting that PrP(C) may regulate its own alpha-cleavage through modulating ADAM8 activity.

9. ADAM-8 appears to favour allergen-induced acute airway inflammation by promoting dendritic cell recruitment and CCL11 and CCL22 production.

10. ADAM8 knockout mice did not display a bone phenotype in vivo but they did not increase RANKL production, OCL formation, or calvarial fibrosis in response to tumor necrosis factor alpha (TNF-alpha) in vivo.

11. ADAM8 is involved in T cell maturation in the medulla but has a relatively minor impact on T cell development.

12. It regulates onset of blood cirlation. (review)

13. The results of this study indicated an essential role for ADAM8 in modulating TNF-alpha signaling in CNS diseases

14. The study finds an increase in retinal re-vascularization but fewer neovascular tufts in the oxygen-induced retinopathy model and increased growth of heterotopically injected tumor cells in Adam8-/- mice compared with wild-type controls.

15. ADAM8 plays a proinflammatory role in airway inflammation.

16. ADAM8 processing by autocatalysis leads to a potential sheddase and to a form of ADAM8 with a function in cell adhesion

17. ADAM8 could contribute to ectodomain shedding of CD23 and may thus be a potential target for therapeutic intervention in allergy and inflammation.

18. Adam8 was identified as the command gene of the group in WT (WildType) and Mmp2 in KO (connexin43-null) mice.

19. ADAM8 plays an important role in physiological and pathological cell interactions by a specific release of functional cell adhesion molecule CHL1 from the cell surface

20. ADAM8 is an allergen-, IL-4-, and IL-13-induced gene in the experimental asthmatic lung. Taken together with the role of ADAM33 in asthma, these results suggest that allergic lung responses involve the interplay of diverse members of the ADAM family