Mouse HVEM / TNFRSF14 Protein (His & Fc Tag)

Atar,HveA,Hvem,Tnfrs14

100ug (NPP3353) Please inquiry

Catalog Number	P10567-M03H
Organism Species	Mouse
Host	Human Cells
Synonyms	Atar,HveA,Hvem,Tnfrs14
Molecular Weight	The recombinant mouse HVEM/Fc is a disulfide-linked homodimeric Protein after removal of the signal peptide. The reduced monomer consists of 415 amino acids and predicts a molecular mass of 46.4 kDa. By SDS-PAGE under reducing conditions, the apparent molecular mass of rmHVEM/Fc monomer is approximately 65 kDa due to the glycosylation.
predicted N	Pro 40
SDS-PAGE
Purity	> 90 % as determined by SDS-PAGE
Protein Construction	A DNA sequence encoding the extracellular domain (Met 1-Gln 206) of mouse HVEM (NP_849262.1) precursor was fused with C-terminal His-tagged Fc region of human IgG1 at the C-terminus.
Bio-activity	Measured by its binding ability in a functional ELISA. Immobilized mouse HVEM-Fch (P10567-M03H）at 10 μg/mL (100 μl/well) can bind biotinylated mouse BTLA-Fc (P51060-M02H)，The EC₅₀ of biotinylated mouse BTLA-Fc (P51060-M02H) is 64-96 ng/mL.
Research Area	Cardiovascular \|Angiogenesis \|Cytokines / Chemokines in Angiogenesis \|TNF Superfamily \|Processes Regulated by TNF Superfamily Members \|Regulation of Natural Killer Cell Co-stimulation by TNF Superfamily Members \|
Formulation	Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background	Herpesvirus entry mediator (HVEM), also referred to as TNFRSF14, TR2 (TNF receptor-like molecule) and ATAR (another TRAF-associated receptor), is a member of type I transmembrane protein belonging to the TNF-receptor superfamily. It is expressed on many immune cells, including T and B cells, NK cells, monocytes, and neutrophils. Two TNF superfamily ligands lymphotoxin α (TNF-β) and LIGHT (TNFSF14) are identified as cellular ligands for HVEM and initiate the positive signaling. However, recent studies have revealed that HVEM is also involved in the unique inhibitory signaling pathway for T cells through activating tyrosine phosphorylation of the immunoreceptor tyrosine-based inhibitory motif (ITIM) in B and T lymphocyte attenuator (BTLA). HVEM provides a stimulatory signal following engagement with LIGHT (TNFSF14) on T cells. In contrast, it can also provide an inhibitory signal to T cells when it binds the B and T lymphocyte attenuator (BTLA), a ligand member of the Immunoglobulin (Ig) superfamily. Thus, HVEM may be viewed as a molecular switch, capable of facilitating both stimulatory and inhibitory cosignaling in T cells. Substantial evidence from both human disease and from experimental mouse models has indicated that dysregulation of the LIGHT-HVEM-BTLA cosignaling pathway can cause inflammation in the lung and in mucosal tissues.
Reference	Murphy KM, et al. (2006) Balancing co-stimulation and inhibition with BTLA and HVEM. Nat Rev Immunol. 6(9): 671-81. Heo SK, et al. (2007) HVEM signaling in monocytes is mediated by intracellular calcium mobilization. J Immunol. 179(9): 6305-10. Steinberg MW, et al. (2008) A crucial role for HVEM and BTLA in preventing intestinal inflammation. J Exp Med. 205(6): 1463-76. Pasero C, et al. (2009) A role for HVEM, but not lymphotoxin-beta receptor, in LIGHT-induced tumor cell death and chemokine production. Eur J Immunol. 39(9): 2502-14. Cheung TC. Modulation of T cell proliferation through the LIGHT-HVEM-BTLA cosignaling pathway. Recent Pat DNA Gene Seq. 3(3): 177-82.