Herpesvirus entry mediator (HVEM) is a type I membrane protein in the TNF receptor superfamily, and it can both promote and inhibit T cell activity. HVEM is highly expressed on naïve CD4+ T cells, CD8+ T memory cells, regulatory T cells, dendritic cells, monocytes, and neutrophils. It functions as a receptor for BTLA, CD160, LIGHT/TNFSF14, and Lymphotoxin-alpha. Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation and contributes to Th1 inflammation and cardiac allograft rejection. In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation and dampens intestinal inflammation. HVEM enhances the development of CD8+ T cell memory and Treg function. It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epitheilal integrity and host defense. The herpesvirus envelope glycoprotein gD, which binds HVEM to initiate membrane fusion, can antagonize both BTLA and LIGHT binding.
Pack Size | Availability | Price/USD | Quantity |
---|---|---|---|
10 μg | 5 days | $ 85.00 | |
50 μg | 5 days | $ 184.00 | |
500 μg | 5 days | $ 825.00 | |
1 mg | 5 days | $ 1,180.00 |
Description | Herpesvirus entry mediator (HVEM) is a type I membrane protein in the TNF receptor superfamily, and it can both promote and inhibit T cell activity. HVEM is highly expressed on naïve CD4+ T cells, CD8+ T memory cells, regulatory T cells, dendritic cells, monocytes, and neutrophils. It functions as a receptor for BTLA, CD160, LIGHT/TNFSF14, and Lymphotoxin-alpha. Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation and contributes to Th1 inflammation and cardiac allograft rejection. In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation and dampens intestinal inflammation. HVEM enhances the development of CD8+ T cell memory and Treg function. It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epitheilal integrity and host defense. The herpesvirus envelope glycoprotein gD, which binds HVEM to initiate membrane fusion, can antagonize both BTLA and LIGHT binding. |
Species | Rhesus macaque |
Expression System | Human Cells |
Tag | C-6His |
Accession Number | F7GSW4 |
Synonyms | TNFRSF14, HVEA, Tumor Necrosis Factor Receptor Superfamily Member 14, Herpes Virus Entry Mediator A, HVEM, Herpesvirus Entry Mediator A, Tumor Necrosis Factor Receptor-Like 2, CD270, TR2 |
Amino Acid | Leu39-Val203 |
Construction | Recombinant Rhesus Macaque TNF Receptor Superfamily Member 14 is produced by our Mammalian expression system and the target gene encoding Leu39-Val203 is expressed with a 6His tag at the C-terminus. |
Protein Purity | Greater than 95% as determined by reducing SDS-PAGE. (QC verified) |
Molecular Weight | 22-40 KDa, reducing conditions |
Endotoxin | Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test. |
Formulation | Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4. |
Reconstitution | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
Stability & Storage |
Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
Shipping |
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature listed below. |
Research Background | Herpesvirus entry mediator (HVEM) is a type I membrane protein in the TNF receptor superfamily, and it can both promote and inhibit T cell activity. HVEM is highly expressed on naïve CD4+ T cells, CD8+ T memory cells, regulatory T cells, dendritic cells, monocytes, and neutrophils. It functions as a receptor for BTLA, CD160, LIGHT/TNFSF14, and Lymphotoxin-alpha. Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation and contributes to Th1 inflammation and cardiac allograft rejection. In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation and dampens intestinal inflammation. HVEM enhances the development of CD8+ T cell memory and Treg function. It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epitheilal integrity and host defense. The herpesvirus envelope glycoprotein gD, which binds HVEM to initiate membrane fusion, can antagonize both BTLA and LIGHT binding. |
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HVEM Protein, Rhesus macaque, Recombinant (His) TNFRSF14 TNFRSF-14 HVEA TR 2 Tumor Necrosis Factor Receptor Superfamily Member 14 Herpes Virus Entry Mediator A HVEM CD 270 Herpesvirus Entry Mediator A TR-2 TNFRSF 14 Tumor Necrosis Factor Receptor-Like 2 CD270 TR2 CD-270 recombinant recombinant-proteins proteins protein