PD-1 (EH33) Mouse mAb #43248
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Mouse IgG2a |
Application Key:
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| IHC Leica Bond | 1:100 |
| Immunohistochemistry (Paraffin) | 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
For a carrier-free (BSA and Azide) version of this product see product #60847.
Protocol
Specificity / Sensitivity
PD-1 (EH33) Mouse mAb recognizes transfected and endogenous levels of total PD-1 protein by immunohistochemistry on formalin-fixed paraffin-embedded tissue sections.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human PD-1 protein.
Background
The programmed cell death 1 protein (PD-1, PDCD1, CD279) is a member of the CD28 family of immunoreceptors that regulate T cell activation and immune responses (1-3). The PD-1 protein contains an extracellular Ig V domain, a transmembrane domain, and a cytoplasmic tail that includes an immunoreceptor tyrosine-based inhibitory motif (ITIM) and an immunoreceptor tyrosine-based switch motif (ITSM). PD-1 is activated by the cell surface ligands PD-L1 and PD-L2 (4). Upon activation, PD-1 ITIM and ITSM phosphorylation leads to the recruitment of the protein tyrosine phosphatases SHP-1 and SHP-2, which suppress TCR signaling (5-7). In addition to activated T cells, PD-1 is expressed in activated B cells and monocytes, although its function in these cell types has not been fully characterized (8). The PD-1 pathway plays an important role in immune tolerance (3); however, research studies show that cancer cells often adopt this pathway to escape immune surveillance (9). Consequently, blockade of PD-1 and its ligands is proving to be a sound strategy for neoplastic intervention (10).
- Ishida, Y. et al. (1992) EMBO J 11, 3887-95.
- Shinohara, T. et al. (1994) Genomics 23, 704-6.
- Nishimura, H. et al. (1999) Immunity 11, 141-51.
- Freeman, G.J. et al. (2000) J Exp Med 192, 1027-34.
- Yokosuka, T. et al. (2012) J Exp Med 209, 1201-17.
- Sheppard, K.A. et al. (2004) FEBS Lett 574, 37-41.
- Chemnitz, J.M. et al. (2004) J Immunol 173, 945-54.
- Thibult, M.L. et al. (2013) Int Immunol 25, 129-37.
- Dong, H. et al. (2002) Nat Med 8, 793-800.
- Topalian, S.L. et al. (2012) Curr Opin Immunol 24, 207-12.
Limited Uses
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