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
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.
Product Datasheet
https://www.prosci-inc.com/?datasheet_sku=76-977
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
Curated Selection
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