Recombinant Mouse Integrin alpha E beta 7 Protein, CF

Integrin  alphaE beta7 (also called M290 in mouse and HML-1 in human) is a type I transmembrane adhesion protein. It is composed of an alphaE subunit (epithelial-associated; also designated as CD103) which is expressed as disulfide-linked 150 kDa and 25 kDa heavy and light chains, and a non-covalently associated 130 kDa beta7 glycoprotein subunit (1, 2). Each subunit has a transmembrane sequence and a short cytoplasmic tail. Integrin  alphaE beta7 is the only known integrin family receptor containing the alphaE subunit, while the beta7 subunit is also a component of Integrin  alpha4 beta7 (1-3). The alphaE extracellular domain (ECD) contains 7 beta-propeller domains surrounding an I domain followed by domains called tight, calf-1 and calf-2. An extra X domain, not found in any other alpha integrin, is also present and contains a proteolytic cleavage site (1, 2). The beta7 ECD contains a vWFA domain, which interacts with the alphaE beta-propeller to form a binding domain. The MIDAS motif (metal ion dependent adhesion site) is critical for binding of alphaE beta7 to its ligand, E-Cadherin (4). The 1093 amino acid (aa) mouse alphaE extracellular domain shares 79% and 99% aa sequence identity with human and rat alphaE respectively, while the 704 aa mouse beta7 ECD shares 87% and 94% aa identity with human and rat beta7, respectively. Integrin alphaE beta7 is mainly restricted to mucosal tissues, where it engages E-Cadherin (4-6). It was first identified as a marker of intestinal intra-epithelial lymphocytes (1, 5, 6). It has since been recognized that a variety of leukocytes, such as cytotoxic CD8⁺ T cells, some dendritic cells, and effector/memory-like regulatory T cells, acquire Integrin  alphaE beta7 in the days following their migration to epithelium in the intestines, lungs, and tonsils (6-13). In these tissues Integrin alphaE beta7 facilitates immune surveillance, including the destruction of infected or transformed epithelial cells and the induction of T cell adaptive responses (7-13). Pathologically, Integrin alphaE beta7 may be involved in allograft rejection of transplanted pancreatic islets and other tissues (14).