Anti-ALK / Anaplastic Lymphoma Kinase, clone ALK/1504

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced) and 0.05% sodium azide. The wild-type anaplastic lymphoma kinase (ALK) protein is a 200kDa transmembrane receptor tyrosine kinase. Its expression is restricted to a few scattered cells in the nervous system (some glial cells and neurons, and a few endothelial cells and pericytes. The hybrid gene,áNPM-ALK, created by the t(2,5)(p23,q35) chromosomal translocation encodes part of the nucleolar phosphoprotein, nucleophosmin (NPM), joined to the entire cytoplasmic portion of the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase. As a consequence, the ALK gene comes under the control of the NPM promoter, which induces a permanent and ubiquitous transcription of the NPM-ALK hybrid gene, resulting in the production of a 80kDa NPM-ALK chimeric protein. This translocation is found in anaplastic large cell lymphomas (ALCL). Reportedly, expression of ALK indicates a better prognosis. Approximately 5%-10% of non-small cell lung carcinomas also express ALK protein producing a cytoplasmic staining pattern. This MAb also reacts with blood vessels that serves as an internal positive control. Protein function: Neuronal receptor tyrosine kinase that is essentially and transiently expressed in specific regions of the central and peripheral nervous systems and plays an important role in the genesis and differentiation of the nervous system. Transduces signals from ligands at the cell surface, through specific activation of the mitogen-activated protein kinase (MAPK) pathway. Phosphorylates almost exclusively at the first tyrosine of the Y- x-x-x-Y-Y motif. Following activation by ligand, ALK induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. Acts as a receptor for ligands pleiotrophin (PTN), a secreted growth factor, and midkine (MDK), a PTN-related factor, thus participating in PTN and MDK signal transduction. PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation. MDK-binding induces phosphorylation of the ALK target insulin receptor substrate (IRS1), activates mitogen-activated protein kinases (MAPKs) and PI3-kinase, resulting also in cell proliferation induction. Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase. Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK. [The UniProt Consortium]