CD279 Antibody [J43.1] (PE)

• 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.

• NCBI Gene ID:

  18566

• Swiss Prot:

  Q02242

• Host:

  Hamster

• Reactivity:

  Mouse

• Clonality:

  Monoclonal

• Clone:

  J43.1

• Conjugation:

  PE

• Type:

  Primary Antibodies

• Field of Research:

  Immunology, Apoptosis

• Purification:

  The monoclonal antibody was purified utilizing affinity chromatography and unreacted dye was removed from the product.

• Concentration:

  Batch dependent

• Buffer:

  Phosphate-buffered aqueous solution, ≤0.09% Sodium azide, may contain carrier protein/stabilizer, ph7.2.

• Modification:

  None

• Shipping Conditions:

  Blue Ice

• Storage Conditions:

  The product should be stored undiluted at 4˚ C and should be protected from prolonged exposure to light. Do not freeze.

• Fragment:

  Armenian Hamster IgG

• 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.

• Symbol:

  Pdcd1

• NCBI Official Name:

  Programmed cell death 1

• NCBI Organism:

  Mus musculus

• Background Reference 01:

  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.

• Background Reference 02:

  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.

• Background Reference 03:

  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.

• Other Product Names:

  PD-1, Pdc1, Ly101, Pdcd1

• Tested Applications:

  Flow

• Physical Properties:

  Liquid