Name: Human HVEM/TNFRSF14 Recombinant Protein (His Tag)

Synonyms: Tumor Necrosis Factor Receptor Superfamily Member 14;Herpes Virus Entry Mediator A;Herpesvirus Entry Mediator A;HveA;Tumor Necrosis Factor Receptor-Like 2;TR2;CD270;TNFRSF14;HVEA;HVEM

Expression host: HEK293 Cells

Sequence: Leu39-Val202

Accesstion: Q92956

Species: Human

Mol_Mass: 18.4 kDa

AP_Mol_Mass: 28 kDa

Tag: C-His

Purity: > 95 % as determined by reducing SDS-PAGE.


Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Formulation: Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.Please refer to the specific buffer information in the printed manual.

Reconstitution: Please refer to the printed manual for detailed information.

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 na?ve 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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