Western blot analysis of extracts from mouse brain, mouse colon, and mouse lung using Integrin β8 (D1V7M) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Integrin β8 (D1V7M) Rabbit mAb recognizes endogenous levels of total integrin β8 protein.
Monoclonal antibody is produced by immunizing animals with recombinant mouse integrin β8 protein.
Integrin α5β8 facilitates activation and release of TGF-β, which has immunosuppressive effects (1). Deletion of integrin β8 from dendritic cells led to development of inflammatory bowl disease and autoimmunity in mice, as well as failure to induce regulatory T cells that require TGF-β for development (2). TGF-β is also involved in Th17 cell differentiation. Mice lacking expression of integrin β8 on dendritic cells fail to develop Th17 cells and are protected from Th17-mediated autoimmune disease (3). Regulatory T cells express high levels of integrin α5β8, which enables them to suppress pathogenic T cell activation by activating latent TGF-β (4). Integrin β8 is also essential for vascular morphogenesis as integrin β8-deficient mice are embryonic or perinatal lethal and exhibit insufficient and abnormal vascular morphogenesis (5).
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