EC Number   |
General Information |
Reference |
|---|
   3.4.24.B9 | malfunction |
silencing of ADAM-9 in melanoma cells significantly reduces cell adhesion to fibroblasts. Ablation of ADAM-9 in fibroblasts almost completely abolishes these cellular interactions and melanoma cell invasion in vitro |
719997 |
| 3.4.24.B9 | more |
ADAM9 is a widely expressed and particularly polyvalent member of the multifunctional ADAM family of proteins |
710800 |
| 3.4.24.B9 | more |
promoter polymorphisms, which regulate ADAM9 transcription, are protective against sporadic Alzheimer's disease |
713107 |
| 3.4.24.B9 | physiological function |
aberrant overexpression of ADAM9 is found in both gastric cancer tissues and cell lines. Knockdown of ADAM9 in gastric cancer SGC-7901 cells induces a dramatic suppression of cell proliferation along with the arrest of the cell cycle in the G0/G1 phase. The 3' untranslated region of ADAM9 mRNA may be bound by miR-126, a suppressor in gastric cancer. Overexpression of miR-126 significantly downregulates ADAM9 in the gastric cancer cells |
754948 |
| 3.4.24.B9 | physiological function |
ADAM-9 interaction with alpha6beta1 integrin regulates fibroblast motility, and alpha6beta1 integrin can induce the mobility of several cell types including macrophages. ADAM-9 is involved in advanced human atherosclerosis and might play roles in the monocyte homing, migration, or proliferation in aorta, carotid, and femoral arteries. ADAM-9 is also involved both in ectodomain shedding and cell interactions through integrin binding. Potential ADAM-9 sheddase substrates include growth factors and cytokines, which are linked to atherosclerosis |
710868 |
| 3.4.24.B9 | physiological function |
ADAM9 enhances the expression of the pro-migratory protein CDCP1 to promote lung metastasis. Endogenous miR-218, which is abundant in normal lung tissue but suppressed in lung tumors, is regulated during the process of ADAM9-mediated CDCP1 expression. Suppression of miR-218 is associated with high migration ability in lung cancer cells |
755410 |
| 3.4.24.B9 | physiological function |
ADAM9 is a member of the ADAM family which is involved in cellular processes like cell adhesion, migration and signalling, involvement of this protease in cervical carcinogenesis, overview |
712114 |
| 3.4.24.B9 | physiological function |
ADAM9 is involved in cell-matrix interactions |
710800 |
| 3.4.24.B9 | physiological function |
Adam9-/- mice are protected from emphysema development, small-airway fibrosis, and airway mucus metaplasia. Cigarette smoke-exposed Adam9-/- mice have reduced lung macrophage counts, alveolar septal cell apoptosis, lung elastin degradation, and shedding of vascular endothelial growth factor receptor-2 and epidermal growth factor receptor in BAL fluid samples |
752452 |
| 3.4.24.B9 | physiological function |
cells lacking ADAM9 show a significant reduction in infection efficiency by encephalomyocarditis virus EMCV. Pharmacological inhibition of the metalloproteinase activity of ADAM9 does not affect virus infection. Reconstitution of inactive ADAM9 in knockout cells restores susceptibility to EMCV. ADAM9 facilitates attachment of EMCV to the cell surface |
754597 |
