Thermo Fisher Scientific CD40 Monoclonal Antibody (1C10), Biotin, eBioscience

Applications and Tested Dilution

Product Specifications

Additional Formats

• Unconjugated
• APC
• Brilliant UV 661
• Brilliant Violet 605
• Functional Grade
• PE
• PE-Cyanine5
• PerCP-eFluor 710
• Super Bright 436
• Super Bright 600
• Super Bright 780
• Request custom conjugation

Product Specific Information

The 1C10 monoclonal antibody reacts with mouse CD40, a 45–50 kDa type I transmembrane glycoprotein belonging to the TNFR family. CD40 is expressed by mouse B lymphocytes, follicular dendritic cells, thymic epithelium, and a subset of peripheral T cells. It regulates B cell development and maturation, induces Ig isotype switching, and promotes proliferation while preventing apoptosis in combination with IL-4. Interaction with CD154 (gp39) on T cells is critical for T-B cell crosstalk and immune regulation.

The 1C10 clone has been reported to exhibit agonistic activity both in vitro and in vivo.

Applications Reported: Flow cytometric analysis
Applications Tested: Tested on mouse splenocytes at ≤1 µg/test (100 µL final volume). Optimal titration recommended.
Filtration: 0.2 µm post-manufacturing filtered.

Target Information

CD40 is a single-chain glycoprotein and a member of the TNF/NGF receptor superfamily. It is expressed on all B cells except plasma cells and also on epithelial cells, carcinomas, and lymphoid dendritic cells. CD40 mediates immune and inflammatory responses including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation.

The transcription factor AKNA regulates CD40 expression, while TNFR2 acts as an adaptor protein in CD40 signaling. CD40-CD154 interaction is implicated in amyloid-beta-induced microglial activation, an early event in Alzheimer’s disease. Mutations in CD40 are associated with Type 3 Hyper-IgM immunodeficiency and CD40 ligand deficiency.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.