HVEM/TNFRSF14 Protein, Mouse (HEK293, His-Fc)

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, His-Fc) is a recombinant protein with a C-Terminal Fc label and a C-Terminal His label, It consists of 206 amino acids (M1-Q206) 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-1, but not TGF-β^[4].

HVEM (mouse, 1 µg/mouse; twice a week for the 2 weeks) shows a significant amelioration of cardiac histology in EAM mode mouse^[4].

Mouse

HEK293

C-hFc;C-His

Q80WM9 (M1-Q206)

230979  [NCBI]

Approximately 65 kDa

Greater than 90% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [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]