Recombinant Human HVEM/TNFRSF14 Fc Chimera Protein, CF

When Recombinant Human BTLA (9235-BT) is immobilized at 1 µg/mL (100 µL/well), Recombinant Human HVEM/TNFRSF14 Fc Chimera Protein (Catalog # 11177-HV) binds with an ED50 of 50.0-600 ng/mL.

2 μg/lane of Recombinant Human HVEM/TNFRSF14 Fc Chimera Protein (Catalog # 11177-HV) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 55-75 kDa and 110-150 kDa, respectively.

• Reactivity: Hu
• Applications: Bioactivity
• Format: Carrier-Free

Recombinant Human HVEM/TNFRSF14 Fc Chimera Protein, CF Summary

• Details of Functionality: Measured by its binding ability in a functional ELISA. When Recombinant Human BTLA (Catalog # 9235-BT) is immobilized at 1 µg/mL (100 µL/well), Recombinant Human HVEM/TNFRSF14 Fc Chimera (Catalog # 11177-HV) binds with an ED₅₀ of 50.0-600 ng/mL.
• Source: Human embryonic kidney cell, HEK293-derived human HVEM/TNFRSF14 protein
  

  Human HVEM/TNFRSF14 (Pro37-Val202) Accession # Q92956.3	IEGRMD	Human IgG1 (Pro100-Lys330)
  N-terminus		C-terminus

• Accession #: Q92956.3
• N-terminal Sequence: Pro37
• Structure / Form: Disulfide-linked homodimer
• Protein/Peptide Type: Recombinant Proteins
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Endotoxin Note: <0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

• Dilutions:
  • Bioactivity
• Theoretical MW: 44 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
• SDS-PAGE: 55-75 kDa, under reducing conditions.

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Reconstitution Instructions: Reconstitute at 500 μg/mL in PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Human HVEM/TNFRSF14 Fc Chimera Protein, CF

• ATAR
• CD270 antigen
• CD270
• CD40-like protein
• Herpes virus entry mediator A
• Herpesvirus entry mediator A
• HveA
• HVEM
• HVEMTR2HVEAATAR
• LIGHTR
• TNFRSF14
• tumor necrosis factor receptor superfamily member 14
• tumor necrosis factor receptor superfamily, member 14 (herpesvirus entrymediator)
• Tumor necrosis factor receptor-like 2
• tumor necrosis factor receptor-like gene2

Background

Herpesvirus entry mediator (HVEM), also known as TNFRSF14 and CD270, is a type I membrane protein in the TNF receptor superfamily. Originally identified as important for entry of herpes simplex virus (HSV) through recognition of HSV glycoprotein D (gD), HVEM has been shown to be involved in the regulation of T cell activity (1). Mature human HVEM consists of an extracellular domain (ECD) with four cysteine-rich domains (CRD), a transmembrane segment, and a cytoplasmic region with a TRAF interaction domain (2). The ECD of human HVEM shares 51% amino acid sequence identity with mouse HVEM. HVEM is found on the membrane of various cell types, including hematopoietic and non-hematopoietic cells, with higher expression in the lung, kidney, and liver (3). HVEM is a receptor for the TNF ligand LIGHT, Ig superfamily members BTLA and CD160, as well as Lymphotoxin-alpha and is involved in bidirectional signaling as both a signaling receptor and a ligand for inhibitory receptors (1,4). Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation (5,6). In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation (3,6,7). HVEM enhances the development of CD8+ T cell memory and Treg function (8, 9). It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epithelial integrity and host defense (10). HVEM is being investigated as an immune checkpoint inhibitor as it is commonly mutated in lymphomas, while upregulation leads to disease progression and is associated with poor prognosis (11, 12).

1. Steinberg, M.W. et al. (2011) Immunological reviews 244:169.
2. Liu, W. et al. (2021) J Exp Med. 218:e20211112).
3. Demerlé C. et al. (2021) Front Oncol. 2021 11:682007.
4. del Rio, M.L. et al. (2010) J. Leukoc. Biol. 87:223.
5. Heo, S.K. et al. (2006) J. Leukoc. Biol. 79:330.
6. Cai, G. et al. (2008) Nat. Immunol. 9:176.
7. Gonzalez, L.C. et al. (2005) Proc. Natl. Acad Sci. USA 102:1116.
8. Tao, R. et al. (2008) J. Immunol. 180:6649.
9. Steinberg, M.W. et al. (2013) PLoS One 8:e77992.
10. Shui, J.W. et al. (2012) Nature 488:222.
11. Aubert, N. et al. (2021) Cancers (Basel) 13:3009.
12. Boice, M. et al. (2016) Cell. 167:405.

Bioinformatics

• Uniprot:
  • Q92956.3()