Overview
- Peptide (C)RHTGRLHLRYGKND, corresponding to amino acid residues 86-109 of rat GPR56 (Accession Q8K3V3). Extracellular, N-terminus.
- Rat and mouse brain lysates, human HL-60 promyelocytic leukemia cell and human NK-92 natural killer cell lysates (1:200–1:1000).
- Western blot analysis of rat (lanes 1 and 3) and mouse (lanes 2 and 4) brain lysates:1,2. Anti-GPR56 (extracellular) Antibody (#AGR-047), (1:200).
3,4. Anti-GPR56 (extracellular) Antibody, preincubated with GPR56 (extracellular) Blocking Peptide (#BLP-GR047). - Western blot analysis of human HL-60 promyelocytic leukemia (lanes 1 and 3) and human NK-92 natural killer (lanes 2 and 4) cell line lysates:1,2. Anti-GPR56 (extracellular) Antibody (#AGR-047), (1:200).
3,4. Anti-GPR56 (extracellular) Antibody, preincubated with GPR56 (extracellular) Blocking Peptide (#BLP-GR047).
- Human HL-60 promyelocytic leukemia cells (5 µg).
GPR56 (ADGRG1) is a member of the adhesion G-protein coupled receptor (GPCR) family, responsible for the regulation of cell adhesion, migration, polarity, and guidance. GPR56 levels are increased in many cancer types and seems to be relevant for tumor cell migration and invasion1,2. GPR56 structure is characterized by a long extracellular domain that is involved in cell-to-cell and cell-to-extracellular matrix interactions. The receptor contains a GPS motif, responsible for cleaving the protein. Seven different glycosylation sites along its N-terminal fragment are present1-3.
Expression of Gpr56 mRNA can be found in neuronal progenitor cells of the cerebral cortical ventricular and subventricular zones during periods of neurogenesis. Studies show that GPR56 protein knockdown promotes mesenchymal differentiation of glioma stem-like initiating cells, accompanied by increased radioresistance in vitro and in vivo1-3.
Mutations in GPR56 may cause bilateral frontoparietal polymicrogyria, a cobblestone-like cortical malformation, characterized by overmigrating neurons and the formation of neuronal ectopias on the surface of the brain2,3.