CD272 (BTLA) Mouse anti-Human, PE-CF594, Clone: J168-540, BD
Mouse Monoclonal Antibody
Manufacturer: BD Biosciences 564801
The J168-540 monoclonal antibody specifically binds to human CD272, also known as BTLA (B and T lymphocyte attenuator), an inhibitory receptor expressed in bone marrow and thymus on developing B and T cells. In the periphery, BTLA is expressed by B cells, T cells, bone marrow-derived dendritic cells, and macrophages. After T cell activation, BTLA appears to be expressed at higher levels on Th1 cell populations than in Th2 cell populations. Upon binding the herpesvirus entry mediator (HVEM/LIGHT-R/CD270), CD272 undergoes tyrosine phosphorylation and inhibits T cell proliferation in a BTLA-dependent manner. CD272 has structural similarities to two other lymphocyte inhibitory receptors, CTLA-4 and PD-1 and is a member of the CD28-like family of coreceptors. Based on these observations, CD272 is considered to be a negative regulator of lymphocyte activation and/or function.
This antibody is conjugated to BD Horizon PE-CF594, which has been developed exclusively by BD Biosciences as a better alternative to PE-Texas Red™. PE-CF594 excites and emits at similar wavelengths to PE-Texas Red™ yet exhibits improved brightness and spectral characteristics. Due to PE having maximal absorption peaks at 496nm and 564nm, PE-CF594 can be excited by the blue (488-nm), green (532-nm) and yellow-green (561-nm) lasers and can be detected with the same filter set as PE-Texas Red™ (eg, 610/20-nm filter).
|Aqueous buffered solution containing BSA and ≤0.09% sodium azide.|
|BTLA1; B- and T-lymphocyte-associated protein|
|Human BTLA Recombinant Protein|
|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