protein

HVEM/TNFRSF14 Protein, Human (Sf9, Fc)

HY-P7366

10 μg;50 μg

90;190 USD

HVEM/TNFRSF14 Protein, Human (Sf9, Fc)

proteins

Sf9 insect cells

10 μg;50 μg

90;190 USD

385326032

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, Human (Sf9, Fc) is a recombinant protein consisting of 146 amino acids (L39-K184) and is produced in Sf9 insect cells.

Human

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] .

rHuHVEM, Fc Chimera; TNFRSF14; TR2; CD270; HVEA

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

Lyophilized after extensive dialysis against PBS.

Room temperature in continental US; may vary elsewhere.