一种DNA损伤和应激诱导的G蛋白偶联受体使细胞停滞在G2/M期。
A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M.
作者信息
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
机构信息
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12334-9. doi: 10.1073/pnas.95.21.12334.
Abstract
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.
摘要
细胞周期进程由高度协调的检查点机制监控，该机制被激活以诱导细胞周期停滞，直到诸如DNA损伤等缺陷得到纠正。我们分离出一种名为G2A（G2期积累）的抗增殖细胞周期调节因子，它主要在未成熟的T和B淋巴细胞祖细胞中表达，是七跨膜G蛋白偶联受体家族的成员。G2A的过表达减弱了BCR-ABL和其他癌基因的转化潜能，并导致细胞在G2/M期积累，且不依赖于p53和c-Abl。G2A可在淋巴细胞中被多种刺激诱导产生，在非淋巴细胞系或组织中诱导程度较低，这些刺激包括不同类型的DNA损伤剂，它作为对损伤和细胞刺激的一种反应，其作用是减缓细胞周期进程。
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