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Integrin alpha 7 beta 1, Recombinant, Mouse, aa34-1033 (VLA-7, Very Late Antigen-7)

Cat no: 145812

Integrin alpha 7 beta 1, Recombinant, Mouse, aa34-1033 (VLA-7, Very Late Antigen-7)

Integrin alpha7beta1, also called VLA-7 (very late antigenпїЅ7), is the major lamininпїЅbinding integrin in cardiac and skeletal muscle (1-4). The non-covalent heterodimer is composed of ~150kD alpha7 and 130kD 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 1116-1160aa 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 (3пїЅ5). The beta1 vWFA domain participates with the alpha7 FGпїЅGAP 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 93пїЅ94% with human, bovine, porcine, ovine, canine and feline beta1. The alpha7 heavy chain in species other than mouse may also be cleaved at aa603-605 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 alpha7beta1 to laminin-111 accounts for many of its effects, but alpha7beta1 also binds most other laminins (5). It protects muscle from exerciseпїЅinduced damage, and its absence in humans or mice causes a form of muscular dystrophy (7-9). alpha7beta1 is also expressed in vascular smooth muscle (VSM), and is important for development of the cerebral vasculature (10). VSM cells show increased alpha7beta1 expression and enhanced laminin binding in injuryпїЅinduced atherosclerosis or PDGF treatment (11, 12). Deletion of alpha7 results in VSM hyperplasia, especially in response to injury (13).\n\nSource:\nRecombinant protein corresponding to aa34-1033 from mouse Integrin alpha 7 beta 1, CHO-derived.\n\nMolecular Weight:\n~123-157kD\n\nEndotoxin:\n<0.01EU/1ug (LAL method)\n\nStorage and Stability:\nLyophilized powder may be stored at -20 degrees C. Stable for 12 months at -20 degrees C. Reconstitute in sterile PBS. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Reconstituted product is stable for 12 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

145812

Size

50ug

Form

Supplied as a lyophilized powder in PBS. BSA free. Reconstitute in 400ug/ml PBS.

Purity

~95% (SDS-PAGE)

References

1. Takada, Y. et al. (2007) Genome Biol. 8:215. 2. Luo, B

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