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ADAM17 (disintegrin and metalloproteinase domain-containing protein 17) cleaves the membrane bound precusor of TNF-alpha to its mature soluble form. ADAM 17 is responsbile for the proteolytical release of soluble JAM3 from endothelial cells surface and the proteolytic release of several other cell-surface proteins, including p75 TNF-receptor, interleukin receptor type II, p55 TNF-receptor, transforming growth factor-alpha, L-selectin, growth hormone receptor, MUC1, and the amyloid precursor protein. It acts as an activator of the Notch pathway by mediating cleavage of Notch and generating the membrane-associated intermediate fragment called Notch extracellular truncation (NEXT). Mutations in the gene can result in inflammatory skin and bowel disease, neonatal 1.
a disintegrin and metallopeptidase domain 17; a disintegrin and metalloprotease domain 17; a disintegrin and metalloproteinase; a disintegrin and metalloproteinase domain 17; a disintegrin and metalloproteinase domain 17 (tumor necrosis factor, alpha, converting enzyme); ADAM; ADAM 17; ADAM metallopeptidase domain 17; ADAM metallopeptidase domain 18; Adam17; ADAM18; ADAMs; CD156B; CD156b antigen; CSVP; Disintegrin and metalloproteinase domain-containing protein 17; metalloendopeptidases; NISBD; NISBD1; Snake venom-like protease; TACE; TNF-alpha convertase; TNF-alpha converting enzyme; TNF-alpha-converting enzyme; tumor necrosis factor, alpha, converting enzyme
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