CXCR5 Rat anti-Mouse, Brilliant Violet 650, Clone: 2G8, BD
Rat Monoclonal Antibody
Manufacturer: BD Biosciences 563981
The 2G8 monoclonal antibody specifically binds to the mouse CXC chemokine receptor, CXCR5. CXCR5 is also known as CD185, BLR1, NLR and MDR15. CXCR5 is a seven-transmembrane, G-protein-coupled receptor that is specific for the CXC chemokine, CXCL13/BLC/BCA-1. The expression of CXCR5 has been detected in spleen, lymph nodes, tonsils, brain, bone marrow, T cells, B cells, cerebrum, cerebellum, hippcampus and pituitary. In mouse spleen, CXCR5 was strictly expressed by mature B cells and a small subset of T lymphocytes. CXCR5 plays a role in directing the migration of B and T cells to B cell follicles with the spleen and certain other lymphoid tissues. The immunogen used to generate 2G8 hybridoma was a recombinant protein containing N-terminal amino acids of mouse CXCR5 (GST-NmBLR1).
The antibody was conjugated to BD Horizon BV650 which is part of the BD Horizon Brilliant Violet family of dyes. This dye is a tandem fluorochrome of BD Horizon BV421 with an Ex Max of 405-nm and an acceptor dye with an Em Max at 650-nm. BD Horizon BV650 can be excited by the violet laser and detected in a filter used to detect APC-like dyes (eg, 660/20-nm filter). Due to the excitation and emission characteristics of the acceptor dye, there will bespillover into the APC and Alexa Fluor 700 detectors. However, the spillover can be corrected through compensation as with any other dye combination.
|Brilliant Violet 650|
|Aqueous buffered solution containing BSA and ≤0.09% sodium azide.|
|CD185; CXC-R5; CXCR-5; C-X-C chemokine receptor type 5; Blr1; MDR15; Gpcr6|
|Store undiluted at 4°C and protected from prolonged exposure to light. Do not freeze.|
We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.
Your feedback has been submitted. Fisher Scientific is always working to improve our content for you. We appreciate your feedback.Ok