Background information
G2A (for G2 accumulation) is a seven transmembrane G protein-coupled receptor that is upregulated in response to DNA damage and stress (1). G2A is predominantly expressed in hematopoietic tissues and in hematopoietic stem cells, and it is more highly detected in pro-B cells, while lower expression is observed in immature B cells and pre-B cells (1,2). G2A is expressed throughout T cell maturation, and it is further increased in response to T-cell activation (3). Ectopic expression of a G2A fusion protein in NIH/3T3 fibroblasts induces a cell cycle arrest that is consistent with a block at the G2/M transition (1,4). G2A is also able to attenuate the proliferative effects of Bcr-Abl, a chimeric tyrosine kinase oncogene, suggesting that G2A possesses anti-oncogenic properties (5). The amino acid sequence of G2A contains a destruction box motif that is consistently observed in cyclins, where it is required for ubiquitination and proteolytic degradation (6).
