EC Number   |
Protein Variants |
Reference |
|---|
   3.4.24.B9 | more |
ADAM9 genomic sequence and mutation analysis determining single-nucleotide polymorphisms, ADAM9 is associated with the gPRA candidate locus for generalized progressive retinal atrophy, a group of inherited retinal diseases which are associated with gradual vision loss in various dog breeds, determined by genome-wide homozygosity mapping using SNP arrays and fine mapping of candidate regions. Mapping the gPRA locus and identification of an ADAM9 partial deletion, overview |
713024 |
| 3.4.24.B9 | more |
construction of a GST-enzyme disintegrin domain fusion protein |
649562 |
| 3.4.24.B9 | more |
construction of several deletion mutants lacking amino acids of the cytoplasmic region by site-directed mutagenesis |
650963 |
| 3.4.24.B9 | more |
enzyme expression in tumor cell lines induces a highly invasive phenotype, protease activity of enzyme is required for invasion |
668152 |
| 3.4.24.B9 | more |
enzyme overexpression in A-549 and EBC-1 cells results in increased invasive capacity in response to nerve growth factor, increased adhesion to brain tissue, and increased expression of integrin alpha3 and beta1 subunits. Administration of enzyme overexpressing A-549 cells to mice results in micrometastatic foci in brain and multiple metastatic colonies in the lungs |
668145 |
| 3.4.24.B9 | more |
enzyme-deficient W10 animals, tumors are well-differentiated, whereas enzyme wild-type W10 animals show predominantly poorly differentiated, and in some cases significantly larger, tumors |
668155 |
| 3.4.24.B9 | more |
expression of intact enzyme and a series of deletion constructs sequentially lacking the metalloprotease domain and the disintegrin domain assembled as chimeras with a C-terminal GFP tag. Stable expression of constructs on the surface of HEK-293 cells significantly decreases adhesion to types I and IV collagen, vitronectin and laminin, but has little effect on adhesion to fibronectin |
667489 |
| 3.4.24.B9 | more |
identification of null mutations in the ADAM metallopeptidase domain 9, ADAM9, gene in four consanguineous families with recessively inherited early-onset cone-rod dystrophy, a group of genetically and phenotypically heterogenous retinal disorders, which is an inherited progressive retinal dystrophy affecting the function of cone and rod photoreceptors, phenotype, overview |
710800 |
| 3.4.24.B9 | more |
overexpression of enzyme enhances growth factor-mediated induction of endocytosis and dynamic recycling of E-cadherin in the human colon cancer cell line HT-29. Enzyme constitutively interacts with E-cadherin, the two proteins co-localize at the plasma membrane |
668504 |
| 3.4.24.B9 | more |
reduced photoreceptor responses occur in Adam9 knockout mice. In 12-month-old knockout mice, photoreceptors appear normal, but the apical processes of the retinal pigment epithelium cells are disorganized and contact between photoreceptor outer segments, POSs, and the RPE apical surface is compromised. In 20-month-old mice, there is clear evidence of progressive retinal degeneration with disorganized POS and thinning of the outer nuclear layer in addition to the anomaly at the POS-RPE junction. RPE basal deposits and macrophages are also apparent in older mice, phenotypes, overview |
710800 |
