Tumor Necrosis Factor Receptor Superfamily, Member 4 (TNFRSF4)

Specification

• Cat#: THP-0269
• Product Name: Tumor Necrosis Factor Receptor Superfamily, Member 4 (TNFRSF4)
• Description: Tumor Necrosis Factor Receptor Superfamily, Member 4 (TNFRSF4), Mouse IgG2a Fc Tag, low endotoxin is expressed from human 293 cells (HEK293). It contains AA Leu 29 - Ala 216. Predicted N-terminus: Leu 29. This protein carries a mouse IgG2a Fc tag at the C-terminus. The protein has a calculated MW of 47.1 kDa. The protein migrates as 58-66 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
• Species: Human
• Molecular Weight: 47.1 kDa
• Source: HEK293
• Introduction: Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor, is a member of the TNFR-superfamily of receptors which is not constitutively expressed on resting naïve T cells, unlike CD28. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. Expression of OX40 is dependent on full activation of the T cell; without CD28, expression of OX40 is delayed and of fourfold lower levels. An artificially created biologic fusion protein, OX40-immunoglobulin (OX40-Ig), prevents OX40 from reaching the T-cell receptors, thus reducing the T-cell response. Experiments in mice have demonstrated that OX40-Ig can reduce the symptoms associated with the cytokine storm (an immune overreaction) while allowing the immune system to fight off the virus successfully. CD134 has been shown to interact with TRAF5 and TRAF2.
• Purity: >95% as determined by SDS-PAGE.
• Formulation: Lyophilized from 0.22 μm filtered solution in 50 mM Tris, 100 mM Glycine, pH7.5. Normally trehalose is added as protectant before lyophilization.

Pharmaceutical Information

• Applications: An artificially created biologic fusion protein, OX40-immunoglobulin (OX40-Ig), prevents OX40 from reaching the T-cell receptors, thus reducing the T-cell response.
• Examples of Clinical Use: reducing the T-cell response
• Affected organisms: Humans