Recombinant Mouse Integrin alpha 7 beta 1 Protein, CF

Integrin  alpha7 beta1, also called VLA‑7 (very late antigen‑7), is the major laminin‑binding integrin in cardiac and skeletal muscle (1‑4). The non‑covalent heterodimer is composed of ~150 kDa alpha7 and 130 kDa beta1/CD29 type I transmembrane glycoprotein subunits with short cytoplasmic tails (2). While alpha7 pairs only with beta1, twelve integrins share the beta1 subunit (1‑5). The longest version of alpha7 is the X1X2B form, encoding 1179 amino acids (aa). Six alternatively spliced 1116‑1160 aa isoforms of the alpha7 subunits have short extracellular (X1, X2) or cytoplasmic (A, C) deletions. Isoforms are differentially expressed by tissue and developmental stage and may show preferences for specific laminins (3‑5). The beta1 vWFA domain participates with the alpha7 FG‑GAP motifs in ligand binding. The alpha7 subunit is cleaved into extracellular heavy and transmembrane/cytoplasmic light chains (3). The mouse alpha7 heavy chain shares 89%, 90%, 87% and 85% aa sequence identity with human, rat, feline and bovine  alpha7, and the mouse beta1 ECD shares 98% aa identity with rat and 93‑94% with human, bovine, porcine, ovine, canine and feline beta1. The alpha7 heavy chain in species other than mouse may also be cleaved at aa 603‑605 by a serine protease; fragments remain associated. This form enhances the active, unfolded and open conformation, promoting cell adhesion and spreading (1, 2, 6). Adhesion of alpha7 beta1 to laminin‑111 accounts for many of its effects, but alpha7 beta1 also binds most other laminins (5). It protects muscle from exercise‑induced damage, and its absence in humans or mice causes a form of muscular dystrophy (7‑9). alpha7 beta1 is also expressed in vascular smooth muscle (VSM), and is important for development of the cerebral vasculature (10). VSM cells show increased alpha7 beta1 expression and enhanced laminin binding in injury‑induced atherosclerosis or PDGF treatment (11, 12). Deletion of alpha7 results in VSM hyperplasia, especially in response to injury (13).