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This purified ABfinity™ recombinant rabbit anti-IR/IGF1R [pY1162/63] monoclonal antibody is specific to human IR/IGF1R [pY1162/63] and does not recognize non-phosphorylated IR/IGF1R. The insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF1R) are heterotetrameric proteins consisting of two ligand-binding alpha subunits and two beta subunits that each contain a tyrosine kinase domain. Based on sequence identity and similarity, reactivity to mouse, rat, chimpanzee, rhesus monkey, swine, equine, bovine, Xenopus, canine, and chicken IR/IGF1R is expected. Rabbit anti-IR/IGF1R [pY1162/63] monoclonal antibody is used in western blotting and ELISA applications.
• Applications: Validated applications for anti-IR/IGF1R [pY1162/63] monoclonal antibody are western blotting and ELISA. • Host Species and Isotype: The host species and isotype of the antibody is rabbit IgG. • Clone ID of Monoclonal Antibody (mAb): The anti-IR/IGF1R [pY1162/62] monoclonal antibody clone is 97H9L7. • Reactivity: Reacts with human IR/IGF1R [pY1162/63]. • Product Size: ABfinity™ Recombinant rabbit anti-IR/IGF1R [pY1162/63] monoclonal antibody is available in a 100 µg size.
Biological actions of insulin and IGF-1 are mediated by their respective cell surface receptor tyrosine kinases that regulate multiple signaling pathways through activation of a series of phosphorylation cascades. The insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF-1R) are heterotetrameric proteins consisting of two ligand-binding alpha subunits and two beta subunits that each contain a tyrosine kinase domain. Insulin/IGF-1 binding to the extracellular domain leads to autophosphorylation of downstream target proteins. These two receptors differ in sequence in regions that confer specificity for the designated ligand as well as in certain intracellular signaling domains, resulting in significant differences in the functional consequences of activation of each receptor. Defects in IR are the cause of various insulin resistance syndromes and IGF-1R defects may cause some forms of growth retardation. Both these signaling cascades are also important for the development of cancer.
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