Recombinant Human HVEM/TNFRSF14/CD270 (C-mFc)

Cat.No.: CW43

Recombinant Human HVEM (C-mFc)
Description
Recombinant Human Herpesvirus entry mediator is produced by our Mammalian expression system and the target gene encoding Pro37-Val202 is expressed with a mFc tag at the C-terminus.
Accession #:Q92956
Known as: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
Formulation
Lyophilized from a 0.2 μm filtered solution of PBS,pH7.4.
Quality Control
Purity:Greater than 95% as determined by reducing SDS-PAGE.
Endotoxin:Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test.
Reconstitution
Always centrifuge tubes before opening. Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100 μg/ml.
Dissolve the lyophilized protein in ddH2O.
Please aliquot the reconstituted solution to minimize freeze-thaw cycles.
Storage
Lyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks.
Reconstituted protein solution can be stored at 4-7°C for 2-7 days.
Aliquots of reconstituted samples are stable at < -20°C for 3 months.
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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