Anti-Mouse CD279 (PD-1) SAFIRE Purified
The J43.1 monoclonal antibody specifically reacts with mouse CD279, also known as PD-1 (programmed death-1), a 50-55 kDa glycoprotein of the Ig superfamily. The PD-1 ligands, PD-L1 (B7-H1) and PD-L2 (B7-H2) are members of the B7 family. Pd-1 contains an Immunoreceptor Tyrosine-based Inhibitory Motif (ITIM) and influences the peripheral tolerances and autoimmune diseases in mice. PD-1 is transiently expressed on CD4/CD8 thymocytes, it is upregulated in apoptotic cells, and it is expressed by activated myeloid and T and B cells.
The binding of PD-1 to its ligands is blocked by the J43 antibody, which also enhances contact hypersensitivity and exacerbates acute Graft-versus-host disease, Experimental autoimmune encephalomyelitis and NOD diabetes. PD-1 seems to downregulate the immune response, as the development of splenomegaly and breakdown of peripheral tolerance in PD-1 deficient mice suggests. Z-VAD-FMK
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Clone
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J43.1
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Format: |
SAFIRE Purified
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Applications
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FC, FA, IHC, IP
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Reactivity
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Mouse
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Isotype:
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Armenian Hamster IgG
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Preperation:
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The product should be stored undiluted at 4°C. Do not freeze. The monoclonal antibody was purified utilizing affinity chromatography. The endotoxin level is determined by LAL test to be less than 0.01 EU/µg of the protein.
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Formulation:
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Phosphate-buffered aqueous solution, ph7.2.
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References:
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Nishimura, H., Agata, Y., Kawasaki, A., Sato, M., Imamura, S., Minato, N., … & Honjo, T. (1996). Developmentally regulated expression of the PD-1 protein on the surface of double-negative (CD4–CD8–) thymocytes. International immunology, 8(5), 773-780. Salama, A. D., Chitnis, T., Imitola, J., Ansari, M. J. I., Akiba, H., Tushima, F., … & Khoury, S. J. (2003). Critical role of the programmed death-1 (PD-1) pathway in regulation of experimental autoimmune encephalomyelitis. The Journal of experimental medicine, 198(1), 71-78. Carreno, B. M., & Collins, M. (2002). The B7 family of ligands and its receptors: new pathways for costimulation and inhibition of immune responses. Annual review of immunology, 20(1), 29-53. |