Overview
- Peptide (C)KGSTLKKAFEHSVHR, corresponding to amino acid residues 429-433 of mouse CD73 (Accession Q61503). Extracellular, N-terminus.
- Mouse and rat brain membranes; human U-87 MG glioblastoma and MDA-MB-231 breast adenocarcinoma cell lysates (1:200–1:1000).
- Western blot analysis of mouse brain membranes (lanes 1 and 3) and rat brain lysate (lanes 2 and 4):1,2. Anti-CD73 (extracellular) Antibody (#ANT-066), (1:200).
3,4. Anti-CD73 (extracellular) Antibody, preincubated with CD73 (extracellular) Blocking Peptide (#BLP-NT066). - Western blot analysis of human U-87 MG glioblastoma cell line lysate (lanes 1 and 3) and human MDA-MB-231 breast adenocarcinoma cell line lysate (lanes 2 and 4):1,2. Anti-CD73 (extracellular) Antibody (#ANT-066), (1:200).
3,4. Anti-CD73 (extracellular) Antibody, preincubated with CD73 (extracellular) Blocking Peptide (#BLP-NT066).
- Mouse brain sections (1:200).
- Human Jurkat T-cell leukemia cells (5 µg).
CD73 (ecto-5′-nucleotidase, NT5E) is a glycosylphosphatidylinositol enzyme expressed on the cell surface of various cell types. CD73 is responsible for hydrolyzing extracellular adenosine monophosphate to adenosine and inorganic phosphate, which results in activation of the G-protein coupled receptors, namely A2AR and A2BR, to exert potent immunoregulatory activity.
CD73 plays an important role in homeostatic functions in healthy organs and tissues. The protein is involved as an inhibitory immune checkpoint molecule, it promotes immune escape of tumor cells since free adenosine generated by the protein inhibits cellular immune responses1,2.
CD73 primarily detected in cancer cells and in immune cells such as CD4+Foxp3+ regulatory T cells, and myeloid-derived suppressor cells that are recruited by the tumor2.
Studies show that CD73 expression is significantly up-regulated in numerous malignant tumors such as breast cancer, colorectal cancer, prostate cancer, ovarian cancer, and gallbladder cancer3.