CD279 Antibody [J43.1] (PE) Cat. No.: 76-977

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psi-iconSpecifications
HOST SPECIES:Hamster
SPECIES REACTIVITY: Mouse
TESTED APPLICATIONS: Flow
SPECIFICITY: 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.

psi-iconProperties
PURIFICATION:The monoclonal antibody was purified utilizing affinity chromatography and unreacted dye was removed from the product.
CLONALITY:Monoclonal
ISOTYPE:Armenian Hamster IgG
CONJUGATE:PE
PHYSICAL STATE:liquid
BUFFER:Phosphate-buffered aqueous solution, ≤0.09% Sodium azide, may contain carrier protein/stabilizer, ph7.2.
CONCENTRATION:batch dependent
STORAGE CONDITIONS:The product should be stored undiluted at 4˚C and should be protected from prolonged exposure to light. Do not freeze.

psi-iconAdditional Info
OFFICIAL SYMBOL:Pdcd1
ALTERNATE NAMES:PD-1, Pdc1, Ly101, Pdcd1
GENE ID:18566
USER NOTE:Optimal dilutions for each application to be determined by the researcher.
psi-iconBackground and References
BACKGROUND: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.
REFERENCES:1) Kubo, T., Uchida, Y., Watanabe, Y., Abe, M., Nakamura, A., Ono, M., ... Takai, T. (2009). Augmented TLR9-induced Btk activation in PIR-Bdeficient B-1 cells provokes excessive autoantibody production and autoimmunity.The Journal of experimental medicine,206(9), 1971-1982.
2) Fukata, M., Breglio, K., Chen, A., Vamadevan, A. S., Goo, T., Hsu, D., ... Abreu, M. T. (2008). The myeloid differentiation factor 88 (MyD88) is required for CD4+ T cell effector function in a murine model of inflammatory bowel disease.The Journal of Immunology,180(3), 1886-1894.
3) Miranda-Hernandez, S., Gerlach, N., Fletcher, J. M., Biros, E., Mack, M., Krner, H., Baxter, A. G. (2011). Role for MyD88, TLR2 and TLR9 but not TLR1, TLR4 or TLR6 in experimental autoimmune encephalomyelitis.The Journal of Immunology,187(2), 791-804.

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