Anti-ADAM17 (human), clone D1(A12) (rec.) (blocking) (Fab Fragment) (His)

ADAM17 (Disintegrin and metalloproteinase domain-containing protein 17), also called TACE (Tumor necrosis factor-alpha-converting enzyme) is the prototype of the ADAM family of ectodomain shedding proteases (sheddase). ADAM17 is understood to be involved in the processing of TNF-alpha at the surface of the cell and from within the intracellular membranes of the trans-Golgi network. This process involves the cleavage and release of a soluble ectodomain from membrane-bound pro-proteins (such as pro-TNF-alpha) and is of known physiological importance. ADAM17 is responsible for the processing of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands and enzymes, including cleaving epidermal growth factor receptor (EGFR) ligands and extracellular Notch1. The proteolytic cleavage is an indispensable activation event for many of these substrates, ADAM17 has emerged as an attractive therapeutic target for the treatment of inflammatory diseases (e.g. rheumatoid arthritis) or inflammation associated cancer. Protein function: Cleaves the membrane-bound precursor of TNF-alpha to its mature soluble form. Responsible for the proteolytical release of soluble JAM3 from endothelial cells surface. Responsible for the proteolytic release of several other cell-surface proteins, including p75 TNF-receptor, interleukin 1 receptor type II, p55 TNF-receptor, transforming growth factor-alpha, L-selectin, growth hormone receptor, MUC1 and the amyloid precursor protein. Acts as an activator of Notch pathway by mediating cleavage of Notch, generating the membrane-associated intermediate fragment called Notch extracellular truncation (NEXT). Plays a role in the proteolytic processing of ACE2. [The UniProt Consortium]