HVEM/TNFRSF14 Protein, Mouse (HEK293, hFc)

HVEM (herpes virus entry mediator, TNFRSF14, CD270) is a member of the tumor necrosis factor receptor superfamily (TNFRSF). HVEM is a bidirectional molecular switch that transduces positive and negative signals. HVEM can deliver proinflammatory and survival signals when engaged by BTLA or LIGHT, stimulating lymphocyte proliferation, activation, and inducing inflammatory reactions. While, HVEM binds to CD160 and BTLA, inhibiting T- and B-lymphocyte activation and proliferation^[2][3]. HVEM/TNFRSF14 Protein, Mouse (HEK293, Fc) is a recombinant protein with a C-Terminal Fc label, It consists of 169 amino acids (Q39-V207) and is produced in HEK293 cells.

HVEM is widely expressed in a range of hematopoietic cells, including B cells, T cells, NK cells, monocytes and immature dendritic cells, and several non-hematopoietic cells and tissues, including the liver, kidney and lung^[1].
The amino acid sequence of human HVEM protein has low homology for mouse HVEM protein.
HVEM is known as the “molecular switch” models of activation and inhibition. HVEM provides an inhibitory or activating signal and bi-directionally regulates host immune function. HVEM binds to LIGHT or LIGHT-α exerts a positive stimulatory effect, stimulating lymphocyte proliferation, activation, and inducing inflammatory reactions; thus, providing a second stimulatory signal for T cell activation. Besides, the Binding of HVEM to BTLA and CD160 exerts an adverse regulatory effect, promoting signal transduction through the ERK1/2 and PI3K (phosphatidylinositol 3-kinase)–AKT (protein kinase B (PKB)) pathways, leading to the production of IFNγ, inhibiting T- and B-lymphocyte activation and proliferation and binding of HVEM to HSV-gD, which can promote HSV infection in target cells^[2][3].
HVEM is considered to be a molecular switch for immune responses, HVEM  induces DCs to produce IL-10 and shows protection against experimental autoimmune myocarditis (EAM) caused by myosin^[4].

HVEM (mouse) induces DCs to produce IL-10, but not TGF-β^[4].

HVEM (mouse, 10 µg/mouse; twice a week for the 2 weeks) shows a significant amelioration of cardiac histology in EAM mode mouse^[4].

1. The ED₅₀ as determined by its ability to bind Human BTLA in functional ELISA is typically 1.17 μg/mL.
2. Measured by its ability to inhibit TNF-beta -mediated cytotoxicity using L-929 mouse fibroblast cells. The ED₅₀ this effect is 1.688 μg/mL in the presence of 50 pg/mL of Recombinant Human TNF-beta, corresponding to a specific activity is 5.92×10² units/mg.

• 
  Measured by its ability to inhibit TNF-beta -mediated cytotoxicity using L-929 mouse fibroblast cells. The ED₅₀ for this effect is 1.688 μg/mL in the presence of 50 pg/mL of Recombinant Human TNF-beta, corresponding to a specific activity is 5.92×10² units/mg.

Mouse

HEK293

C-hFc

Q80WM9 (Q39-V207)

230979  [NCBI]

QPSCRQEEFLVGDECCPMCNPGYHVKQVCSEHTGTVCAPCPPQTYTAHANGLSKCLPCGVCDPDMGLLTWQECSSWKDTVCRCIPGYFCENQDGSHCSTCLQHTTCPPGQRVEKRGTHDQDTVCADCLTGTFSLGGTQEECLPWTNCSAFQQEVRRGTNSTDTTCSSQV

50-65 kDa

• 
  Greater than 95% as determined by reducing SDS-PAGE.
• 
  Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Ma B, et al. High expression of HVEM is associated with improved prognosis in intrahepatic cholangiocarcinoma. Oncol Lett. 2021 Jan;21(1):69.  [Content Brief]

  [2]. Yu X, et al. BTLA/HVEM Signaling: Milestones in Research and Role in Chronic Hepatitis B Virus Infection. Front Immunol. 2019 Mar 29;10:617.  [Content Brief]

  [3]. Rodriguez-Barbosa JI, et al. HVEM, a cosignaling molecular switch, and its interactions with BTLA, CD160 and LIGHT. Cell Mol Immunol. 2019 Jul;16(7):679-682.  [Content Brief]

  [4]. Cai G, et al. Amelioration of myocarditis by HVEM-overexpressing dendritic cells through induction of IL-10-producing cells. Cardiovasc Res. 2009 Dec 1;84(3):425-33.  [Content Brief]