Product Details
| abID | ab155629 |
|---|---|
| Alternate Name | TNFRSF14, ATAR, HVEA, HVEM, LIGHTR, TR2, Tumor necrosis factor receptor superfamily member 14, Herpesvirus entry mediator. |
| Gene Symbol | TNFRSF14 |
| Gene ID | 8764 |
| Accession # | Q92956 |
| Source | HEK293 cells |
| Appearance | Lyophilized |
| Physical Form Description | Lyophilized from 0.22 μm filtered solution in 50 mM tris, 100 mM glycine, pH 7.0. Normally Mannitol or Trehalose is added as protectants before lyophilization. |
| Molecular Weight | This protein is a disulfide-linked homodimeric protein after removal of the signal peptide. The reduced monomer consists of 413 amino. rhHVEM-Fc, fused with the Fc region of human IgG1 at the C-terminus and has a calculated MW of 45.4 kDa expressed. Prote |
| Purity by SDS-PAGE | ≥95% |
| Endotoxin Level | <1 EU/μg by LAL method |
| Biological Activity | Measured by its ability to inhibit TNF-beta-mediated cytotoxicity using L929 Mouse fibrosarcoma cells. The ED50 for this effect is typically 2.5-10 μg/ml in the presence of 1 ng/ml of recombinant human TNF-beta. |
| Reconstitution Instructions | Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 µg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C. |
| Handling | Centrifuge the vial prior to opening. |
| Storage Conditions | -20°C |
| Shipping Conditions | Gel Pack |
| USAGE | For Research Use Only! Not to be used in humans |
Details
Herpesvirus entry mediator (HVEM), also known as TNFRSF14, TR2 (TNF receptor like molecule) and ATAR (another TRAF associated receptor), is a type I membrane protein belonging to the TNF/NGF receptor superfamily. HVEM expression has been detected in peripheral blood T cells, B cells, monocytes and in various tissues enriched in lymphoid cells. The extracellular domain of HVEM has been shown to interact directly with the herpes simplex virus envelope glycoprotein D (gD). Two TNF superfamily ligands, including the secreted TNFβ (lymphotoxin α) and the membrane protein LIGHT (lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes), have been shown to be the cellular ligands for HVEM. Besides HVEM, LIGHT can also interact with LTβR, the receptor for lymphotoxin αβ heterotrimer. The role of the HVEM LIGHT /LTβ receptor ligand pair in immune function and herpesvirus pathobiology remains to be elucidated.
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