Integrin β8 (D1V7M) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0790

Target Information
UniProt ID	Q0VBD0

Product Details
Size	100 µL
Reactivity	Mouse
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with recombinant mouse integrin β8 protein.

Usage
Application	WB
Product Usage Information Dilution	Western Blotting (1:1000)
MW (Target)	98 kDa

Background
Integrin α5β8 facilitates activation and release of TGF-β, which has immunosuppressive effects 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 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 Regulatory T cells express high levels of integrin α5β8, which enables them to suppress pathogenic T cell activation by activating latent TGF-β 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.

Background

Integrin α5β8 facilitates activation and release of TGF-β, which has immunosuppressive effects 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 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 Regulatory T cells express high levels of integrin α5β8, which enables them to suppress pathogenic T cell activation by activating latent TGF-β 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.

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