PD-L1 (Extracellular Domain Specific) (E1J2J™) Rabbit mAb #15165
- WB
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 40-50 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunohistochemistry (Paraffin) | 1:100 |
Storage
For a carrier-free (BSA and azide free) version of this product see product #24224.
Protocol
Specificity / Sensitivity
PD-L1 (Extracellular Domain Specific) (E1J2J™) Rabbit mAb recognizes endogenous levels of total PD-L1 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human PD-L1 protein.
Background
Programmed cell death 1 ligand 1 (PD-L1, B7-H1, CD274) is a member of the B7 family of cell surface ligands that regulate T cell activation and immune responses. The PD-L1 ligand binds the PD-1 transmembrane receptor and inhibits T cell activation. PD-L1 was discovered following a search for novel B7 protein homologs and was later shown to be expressed by antigen presenting cells, activated T cells, and tissues including placenta, heart, and lung (1-3). Similar in structure to related B7 family members, PD-L1 protein contains extracellular IgV and IgC domains and a short, cytoplasmic region. Research studies demonstrate that PD-L1 is expressed in several tumor types, including melanoma, ovary, colon, lung, breast, and renal cell carcinomas (4-6). Expression of PD-L1 in cancer is associated with tumor-infiltrating lymphocytes, which mediate PD-L1 expression through the release of interferon gamma (7). Additional research links PD-L1 expression to cancers associated with viral infections (8,9).
- Dong, H. et al. (1999) Nat Med 5, 1365-9.
- Freeman, G.J. et al. (2000) J Exp Med 192, 1027-34.
- Liang, S.C. et al. (2003) Eur J Immunol 33, 2706-16.
- Dong, H. et al. (2002) Nat Med 8, 793-800.
- Thompson, R.H. et al. (2006) Cancer Res 66, 3381-5.
- Pardoll, D.M. (2012) Nat Rev Cancer 12, 252-64.
- Taube, J.M. et al. (2012) Sci Transl Med 4, 127ra37.
- Lyford-Pike, S. et al. (2013) Cancer Res 73, 1733-41.
- Chen, B.J. et al. (2013) Clin Cancer Res 19, 3462-73.
Limited Uses
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