Human DcR3 / TNFRSF6B Protein, Fc Tag

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TNB-H5255-50ug
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TNB-H5255-1mg (500ug X 2)
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Synonyms

TNFRSF6B, DCR3, TR6, M68

Source

Human DcR3, Fc Tag (TNB-H5255) is expressed from human 293 cells (HEK293). It contains AA Val 30 - His 300 (Accession # O95407-1).

Predicted N-terminus: Val 30

Molecular Characterization

This protein carries a human IgG1 Fc tag at the C-terminus.

The protein has a calculated MW of 56.2 kDa. The protein migrates as 60-65 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

Endotoxin

Less than 1.0 EU per μg by the LAL method / rFC method.

Purity

>90% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in Tris with Glycine, Arginine and NaCl, pH7.5 with trehalose as protectant.

Contact us for customized product form or formulation.

Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.

Background Introduction

Tumor necrosis factor receptor superfamily member 6B (TNFRSF6B) is also known as Decoy Receptor 3 (DcR3), Decoy receptor for Fas ligand and M68, which belongs to the tumor necrosis factor receptor superfamily. TNFRSF6 is a soluble protein which contains four TNFR-Cys repeats. Unlike most of the other members of TNFR superfamily, TNFRSF6 is a soluble protein which contains no transmembrane domain. TNFRSF6B acts as a decoy receptor that competes with death receptors for ligand binding. The protein is postulated to play a regulatory role in suppressing FasL- and LIGHT-mediated cell death and T cell activation as well as to induce angiogenesis via neutralization of TL1A.