HVEM Protein, Human, Recombinant (His & Fc Tag)

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HVEM Protein, Human, Recombinant (His & Fc Tag): Product Information

Purity
> 85 % as determined by SDS-PAGE
Endotoxin
< 1.0 EU per μg of the protein as determined by the LAL method
Activity
Measured by its ability to bind biotinylated mouse BTLA-Fc(Cat:51060-M02H) in functional ELISA.
Protein Construction
A DNA sequence encoding the extracellular domain (Met 1-Val 202) of human HVEM (NP_003811.2) precursor was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus.
Accession#
Expressed Host
HEK293 Cells
Species
Human
Predicted N Terminal
Pro 37
Molecule Mass
The recombinant human HVEM/Fc is a disulfide-linked homodimeric protein after removal of the signal peptide. The reduced monomer consists of 413 amino acids and predicts a molecular mass of 45.4 kDa. By SDS-PAGE under reducing conditions, the apparent molecular mass of rh HVEM/Fc monomer is approximately 60-65 kDa due to glycosylation.
Formulation
Lyophilized from sterile 100mM Glycine, 10mM NaCl, 50mM Tris, pH 7.5
Please contact us for any concerns or special requirements.
Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the hard copy of CoA.
Shipping
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.
Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Stability & Storage
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃
Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Reconstitution
A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

HVEM Protein, Human, Recombinant (His & Fc Tag): Images

HVEM Protein, Human, Recombinant (His & Fc Tag): Alternative Names

ATAR Protein, Human; CD270 Protein, Human; HVEA Protein, Human; HVEM Protein, Human; LIGHTR Protein, Human; TR2 Protein, Human

HVEM Background Information

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.
Full Name
tumor necrosis factor receptor superfamily, member 14
References
  • 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.
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