Product Pathways - Lymphocyte Signaling
IDO Antibody #12006
Reactivity Key: H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
IDO Antibody recognizes endogenous levels of total IDO protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human IDO protein. Antibodies are purified by protein A and peptide affinity chromatography.
Western blot analysis of extracts from HeLa cells, untreated (-) or treated with Human Interferon-γ (hIFN-γ) #8901 (10 ng/ml, 16 hr; +), using IDO Antibody (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing full-length human IDO (hIDO; +), using IDO Antibody.
Immunoprecipitation of IDO from HeLa cells, treated with Human Interferon-γ (hIFN-γ) #8901 (10 ng/ml, 16 hr), using Normal Rabbit IgG #2729 (lane 2) or IDO Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using IDO Antibody.
INDO/IDO1/indoleamine 2,3-dioxygenase (IDO) is an IFN-γ-inducible enzyme that catalyzes the rate-limiting step of tryptophan degradation (1). IDO is upregulated in many tumors and in dendritic cells in tumor-draining lymph nodes. Elevated tryptophan catabolism in these cells leads to tryptophan starvation of T cells, limiting T cell proliferation and activation (2). Therefore, IDO is considered an immunosuppresive molecule, and research studies have shown that upregulation of IDO is a mechanism of cancer immune evasion (3). The gastrointestinal stromal tumor drug, imatinib, was found to act, in part, by reducing IDO expression, resulting in increased CD8+ T cell activation and induction of apoptosis in regulatory T cells (4). In addition to its enzymatic activity, IDO was recently shown to have signaling capability through an immunoreceptor tyrosine-based inhibitory motif (ITIM) that is phosphorylated by Fyn in response to TGF-β. This leads to recruitment of SHP-1 and activatation of the noncanonical NF-κB pathway (5).
- Yasui, H. et al. (1986) Proc Natl Acad Sci U S A 83, 6622-6.
- Mellor, A.L. et al. (2003) Adv Exp Med Biol 527, 27-35.
- Prendergast, G.C. (2008) Oncogene 27, 3889-900.
- Balachandran, V.P. et al. (2011) Nat Med 17, 1094-100.
- Pallotta, M.T. et al. (2011) Nat Immunol 12, 870-8.
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For Research Use Only. Not For Use In Diagnostic Procedures.