HVEM/TNFRSF14 Antibody (2024B) [Alexa Fluor® 405]

• Reactivity: Mu
• Applications: Flow
• Clone: 2024B
• Clonality: Monoclonal
• Host: Rabbit
• Conjugate: Alexa Fluor 405

HVEM/TNFRSF14 Antibody (2024B) [Alexa Fluor® 405] Summary

• Additional Information: Recombinant Monoclonal Antibody.
• Immunogen: Mouse myeloma cell line NS0-derived recombinant mouse HVEM/TNFRSF14
  Gln39-Val207
  Accession # NP_849262
• Specificity: Detects mouse HVEM/TNFRSF14 in direct ELISAs.
• Isotype: IgG
• Clonality: Monoclonal
• Host: Rabbit
• Purity Statement: Protein A or G purified from cell culture supernatant

Applications/Dilutions

• Dilutions:
  • Flow Cytometry 0.25-1 ug/10^6 cells

Packaging, Storage & Formulations

• Storage: Store the unopened product at 2 - 8 °C. Do not use past expiration date.
• Buffer: Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.

Notes

This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.

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

Alternate Names for HVEM/TNFRSF14 Antibody (2024B) [Alexa Fluor® 405]

• 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

HVEM (herpesvirus entry mediator) is a type I membrane protein that is TNF receptor superfamily member 14 (TNFRSF14) (1). The mouse HVEM cDNA encodes a 275 amino acid (aa) protein. It contains a 36 aa signal peptide, a 170 aa extracellular domain with three cysteine rich domains (CRD), a 24 aa transmembrane region and a 45 aa cytoplasmic tail with a TRAF interaction domain (1). HVEM expression is highest on naïve, memory and regulatory T cells, but declines during T cell activation (2, 3). It is present at low levels on most resting leukocytes (4). HVEM is a receptor for the IGSF member BTLA (B and T lymphocyte attenuator), CD160, and the TNF family ligand LIGHT (lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes) (2, 9). HVEM and BTLA are constitutively expressed on T cells, while LIGHT is generally considered to be inducible upon TCR activation. In the absence of activation, HVEM and BTLA interact monomerically, either in cis, or in trans. A same cell (or cis) interaction likely promotes general cell survival, while a between cell (or trans) interaction promotes a state of lymphocyte inactivity through the BTLA cytoplasmic domain. Following T cell activation, LIGHT appears and disrupts existing HVEM-BTLA bonds. A LIGHT-HVEM trimer now forms in trans, initiating HVEM-mediated NF kappa B signaling and a proinflammatory response (10). BTLA and LIGHT interactions are not mutually exclusive, but BTLA appears dominant (4, 6, 7). The herpesvirus envelope glycoprotein gD, which binds HVEM CRD1 to initiate membrane fusion, can antagonize both BTLA and LIGHT binding (1, 6, 7, 9). Human, but not mouse, HVEM can also bind lymphotoxin a within CRD2 3 (9, 11). Graft‑vs‑host disease and Th1 type intestinal inflammation can be ameliorated by interrupting T cell LIGHT/HVEM interactions, while disruption of BTLA/HVEM interaction promotes intestinal inflammation (12-14). Mouse HVEM ECD shares 89% and 53% aa identity with rat and human HVEM, respectively. Mouse HVEM can recognize human BTLA and LIGHT, but human HVEM does not recognize mouse ligands (2, 11).

1. Hsu, H. et al. (1997) J. Biol. Chem. 272:13471.
2. Sedy, J.R. et al. (2005) Nat. Immunol. 6:90.
3. Tao, R. et al. (2008) J. Immunol. 180:6649.
4. Wang, Y. et al. (2005) J. Clin. Invest. 115:711.
5. Nelson, C.A. et al. (2008) J. Immunol. 180:940.
6. Gonzales, L.C. et al. (2005) Proc. Natl. Acad Sci. USA 102:1116.
7. Compaan, D.M. et al. (2005) J. Biol. Chem. 280:39553.
8. Cai, G. et al. (2008) Nat. Immunol. 9:176.
9. Mauri, D.N. et al. (1998) Immunity 8:21.
10. Ware, C.F. (2008) Immunol. Rev. 223:186.
11. Bossen, C. et al. (2006) J. Biol. Chem. 281:13964.
12. Xu, Y. et al. (2007) Blood 109:4097.
13. Wang, J. et al. (2005) J. Immunol. 174:8173.
14. Steinberg, M.W. et al. (2008) J. Exp. Med. 205:1463.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Bioinformatics

• Uniprot:
  • NP_849262(Mouse)