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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M.

Cell cycle progression is monitored by highly coordinated checkpoint machinery, which is activated to induce cell cycle arrest until defects like DNA damage are corrected. We have isolated an anti-proliferative cell cycle regulator named G2A (for G2 accumulation), which is predominantly expressed in immature T and B lymphocyte progenitors and is a member of the seven membrane-spanning G protein-coupled receptor family. G2A overexpression attenuates the transformation potential of BCR-ABL and other oncogenes, and leads to accumulation of cells at G2/M independently of p53 and c-Abl. G2A can be induced in lymphocytes and to a lesser extent in nonlymphocyte cell lines or tissues by multiple stimuli including different classes of DNA-damaging agents and serves as a response to damage and cellular stimulation which functions to slow cell cycle progression.[1]

References

  1. A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M. Weng, Z., Fluckiger, A.C., Nisitani, S., Wahl, M.I., Le, L.Q., Hunter, C.A., Fernal, A.A., Le Beau, M.M., Witte, O.N. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
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