Recombinant Human BST-2/Tetherin Protein, CF

When Recombinant Human BST-2/Tetherin (Catalog # 9939-BS) isimmobilized at 1 µg/mL (100 µL/well), Recombinant Viral Dengue Virus 4 EnvelopeFc Chimera binds with an ED50 of 0.2-1.6 μg/mL.

2 μg/lane of Recombinant Human BST-2/Tetherin (Catalog # 9939-BS) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® blue staining, showing bands at 13 kDa and 31 kDa.

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

Recombinant Human BST-2/Tetherin Protein, CF Summary

• Details of Functionality: Measured by its binding ability in a functional ELISA. When Recombinant Human BST-2/Tetherin is immobilized at 1 µg/mL (100 µL/well), Recombinant Viral Dengue Virus 4 Envelope Fc Chimera (Catalog# 9939-BS) binds with an ED₅₀ of 0.2-1.6 μg/mL.
• Source: E. coli-derived human BST-2/Tetherin protein
  Asn49-Ser161, with an N-terminal Met and C-terminal 6-His tag
• Accession #: Q10589-1
• N-terminal Sequence: Met
• Protein/Peptide Type: Recombinant Proteins
• Purity: >90%, 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: 14 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: 13 kDa and 31 kDa, 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 MES and NaCl with Trehalose.
• Purity: >90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Reconstitution Instructions: Reconstitute at 250 μg/mL in water.

Notes

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

Alternate Names for Recombinant Human BST-2/Tetherin Protein, CF

• bone marrow stromal antigen 2
• bone marrow stromal cell antigen 2
• BST2
• BST-2
• CD317 antigen
• CD317
• HM1.24 Antigen
• NPC-A-7
• PDCA-1
• Tetherin

Background

BST-2, also known as tetherin or CD317, is a type II transmembrane protein that is constitutively expressed in several cell types including T cells, B cells, monocytes and macrophages, as well as on several cancer cell lines including the B cell lineage in multiple myeloma (1, 2). Originally named bone marrow stromal cell antigen 2, BST-2 was identified to inhibit viral replication due to its unusual topology (3-5). The extracellular C-terminus of the protein is modified with GPI (glycosylphosphatidylinositol) membrane anchor, which enables BST-2 to interact at each of its ends with the cell or the viral membrane. The ectodomain of the protein also contains three cysteine residues that can form intermolecular disulfide bonds to form parallel dimers (2). Human BST-2 consists of a 20 amino acid (aa) cytoplasmic domain, a 28 aa transmembrane segment, and a 113 aa extracellular domain (ECD). Within the ECD, human BST-2 shares 41% and 35% aa sequence identity with mouse and rat BST-2, respectively. BST-2 was identified as a major mediator of the innate immune defense against enveloped viruses. BST-2 was shown to interact with formed viral particles tethering them to surface of infected cells, thereby reducing viral release (6). BST-2 inhibits the release of diverse group of enveloped viruses including members of the retrovirus, togavirus, filovirus, arenavirus, flavivirus, rhabdovirus, orthohepadnavirus, orthomyxovirus, poxvirus, paramyxovirus, and herpesvirus families (7-9). The mechanism BST-2 inhibition of viral budding was suggested to be through directly bridging the host and viral membranes through simultaneous embedding of its two opposing membrane anchors (9). To counteract BST-2 functions, many viruses have evolved to develop strategies to antagonize BST-2 function (9, 10). In addition to inhibiting viral release, BST-2 can act as an innate immune sensor of viral infections by acting as a pattern recognition receptor that activates NF-kappa B to induce inflammatory responses through interactions with the immunoglobulin-like transcript 7 (ILT7/LILRA4) (10, 11).

1. Evans, D.T. et al. (2010) Trens Microbiol. 18:388.
2. Ohtomo, T. et al. (1999) Biochem. Biophys. Res. Commun. 258:583.
3. Ishikawa, J. et al. (1995) Genomics. 26:527.
4. Neil, S.J. et al. (2008) Nature. 451:425.
5. Kupzig, S. et al. (2003) Traffic. 4:694.
6. Janvier K. et al. (2012) Curr HIV Res. 10:315.
7. Evans D.T. et al. (2010) Trends Microbiol. 18:388.
8. Mahauad-Fernandez W.D. et al. (2012) Immun Inflamm Dis. 4:4.
9. Swiecki M. et al. (2013) Mol Immunol. 54:132.
10. Sauter D. (2014) Front Microbiol. 5:163.
11. Hotter D. et al. (2013) J Mol Biol. 425:4956.

Bioinformatics

• Uniprot:
  • Q10589-1()