Anti-Adam17

0.5mg/ml if reconstituted with 0.2ml sterile DI water. ADAM17 (ADAM metallopeptidase domain 17), also called TACE (tumor necrosis factor-alpha-converting enzyme), is a 70-kDa enzyme that belongs to the ADAM protein family of disintegrins and metalloproteases. Expression studies showed that the encoded protein cleaves precursor tumor necrosis factor-alpha to its mature form. Northern blot analysis revealed that the gene was expressed as a 5-kb mRNA in all tissues examined. ADAM17 is understood to be involved in the processing of tumor necrosis factor alpha (TNF-a) at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. This process, which is also known as 'shedding', involves the cleavage and release of a soluble ectodomain from membrane-bound pro-proteins (such as pro-TNF-a), and is of known physiological importance. ADAM17 was the first 'sheddase' to be identified, and is also understood to play a role in the release of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands, and enzymes. 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. Plays a role in the proteolytic processing of ACE2. 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 (PubMed:10799547, PubMed:11108241). Acts as an activator of Notch pathway by mediating cleavage of Notch, generating the membrane-associated intermediate fragment called notch extracellular truncation (NEXT) (PubMed:10882063). Plays a role in hemostasis through shedding of GP1BA, the platelet glycoprotein Ib alpha chain (PubMed:12907434). Mediates the proteolytic cleavage of LAG3, leading to release the secreted form of LAG3 (PubMed:17245433). Mediates the proteolytic cleavage of IL6R, leading to the release of secreted form of IL6R. Mediates the proteolytic cleavage and shedding of FCGR3A upon NK cell stimulation, a mechanism that allows for increased NK cell motility and detachment from opsonized target cells. [The UniProt Consortium]