Overview
- Peptide (C)KSDSDRGGHWATEG, corresponding to amino acid residues 499-512 of human CD97/ADGRE5 (Accession P48960). Extracellular, N-terminus.
- Human cell lines: HepG2 liver carcinoma, Jurkat T-cell leukemia, K562 chronic myelogenous leukemia and THP-1 monocytic leukemia cell lines (1:200-1:1000).
Western blot analysis of HepG2 (lanes 1 and 5), Jurkat (lane 2 and 6), K562 (lanes 3 and 7) and THP-1 (lanes 4 and 8) cell lines lysates:1-4. Anti-Human CD97/ADGRE5 (extracellular) Antibody (#AER-055), (1:200).
5-8. Anti-Human CD97/ADGRE5 (extracellular) Antibody, preincubated with Human CD97/ADGRE5 (extracellular) Blocking Peptide (#BLP-ER055).
- Human THP-1 monocytic leukemia cells (2.5 µg/5x105 cells).
CD97, encoded by the adhesion G protein-coupled receptor 5 (ADGRE5) gene, is a member of the epidermal growth factor (EGF) seven transmembrane receptor family, belonging to the adhesion family of G protein-coupled receptors (GPCRs)1. CD97 is widely expressed on the surface of lymphoid cells, macrophages, smooth muscle cells and several types of tumor cells and acts through binding of decay accelerating factor (CD55) and dermatan sulfate2.
In the immune system, CD97 is known as a critical mediator of host defense. Upon lymphoid, myeloid cells and neutrophil activation, CD97 is upregulated to promote adhesion and migration to sites of inflammation3. Antibodies against CD97 have been demonstrated to diminish various inflammatory disorders by depleting granulocytes and the interaction between CD97 and its ligand CD55 regulates T-cell activation and increases proliferation and cytokine production4.
Changes in the expression of CD97 have been described in auto-inflammatory diseases, such as rheumatoid arthritis and multiple sclerosis. Outside the immune system, CD97 is likely involved in cell-cell interactions and ectopic CD97 expression leading to enhanced cell-cell aggregation5.
