CD279 Antibody [J43.1] (PE)

Product Specifications

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

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.