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Recombinant Mouse HVEM/TNFRSF14 Fc Chimera Protein, CF Summary
Details of Functionality
Measured by its binding ability in a functional ELISA. When Recombinant Mouse (rm) HVEM Fc Chimera is immobilized at 100 ng/ mL, 100 μL/well, the concentration of biotinylated rmBTLA Fc Chimera that produces 50% of the optimal binding response is found to be approximately 30-120 ng/mL.
Source
Chinese Hamster Ovary cell line, CHO-derived mouse HVEM/TNFRSF14 protein
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Note
<0.01 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Binding Activity
Theoretical MW
45.6 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS.
Purity
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain
Reconstitution Instructions
Reconstitute at 1 mg/mL in PBS.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Mouse HVEM/TNFRSF14 Fc Chimera Protein, CF
ATAR
CD270 antigen
CD270
CD40-like protein
Herpes virus entry mediator A
Herpesvirus entry mediator A
HveA
HVEM
HVEMTR2HVEAATAR
LIGHTR
TNFRSF14
tumor necrosis factor receptor superfamily member 14
tumor necrosis factor receptor superfamily, member 14 (herpesvirus entrymediator)
Tumor necrosis factor receptor-like 2
tumor necrosis factor receptor-like gene2
Background
HVEM (herpesvirus entry mediator), also known as TNFRSF14 and CD270, is a type I membrane protein in the TNF receptor superfamily, and it can both promote and inhibit T cell activity (1). Mature mouse HVEM consists of a 170 amino acid (aa) extracellular domain (ECD) with three cysteine-rich domains (CRD), a 24 aa transmembrane segment, and a 45 aa cytoplasmic tail with a TRAF interaction domain (2). Within the ECD, mouse HVEM shares 55% and 89% aa sequence identity with human and rat HVEM, respectively. HVEM is highly expressed on naïve CD4+ T cells, CD8+ T memory cells, regulatory T cells, dendritic cells, monocytes, and neutrophils (3-7). Its expression declines during effector T cell activation but is upregulated during Treg activation (3, 4). HVEM functions as a receptor for BTLA, CD160, LIGHT/TNFSF14, and Lymphotoxin-alpha (3, 8-11). Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation (7, 9) and contributes to Th1 inflammation and cardiac allograft rejection (12, 13). In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation (3, 6, 8, 9) and dampens intestinal inflammation (14). HVEM enhances the development of CD8+ T cell memory and Treg function (4, 5). It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epitheilal integrity and host defense (15). The herpesvirus envelope glycoprotein gD, which binds HVEM to initiate membrane fusion, can antagonize both BTLA and LIGHT binding (Montgomery, 8, 10, 16).
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