Bad蛋白磷酸化和剪切修饰对神经胶质瘤细胞凋亡的调控作用*

Phosphorylation and cleavage-modification of Bad on the regulation of cellular apoptosis in glioma cells*

摘要:

Bcl-2相关死亡启动子同源基因编码蛋白Bad是线粒体凋亡通路的开关蛋白。药物处理和各种内源性信号通过改变其特殊位点的磷酸化状态和对其生化构型进行剪切修饰，实现对神经胶质瘤细胞内促凋亡或促生存信号通路的下游调控。Bad还可介导细胞周期蛋白的促凋亡作用，使之与细胞周期阻滞保持一致。Bad不仅是抗胶质瘤药物的作用焦点，也是其基因治疗的理想候选物。

Abstract:

B-cell leukemia/lymphoma-2-associated death promoter homolog (Bad) is a switchable protein of the mitochondria apoptotic pathway. Drug treatment and multiple endogenous signals usually change its phosphorylation status in several specific sites and modify its biological configuration by cleaving into truncated forms so as to accomplish a down-stream regulation of pro-apoptotic or pro-survival signaling pathways in glioma cells. Bad can also mediate the pro-apoptotic effects of cyclins to ensure a consistency of the apoptotic procedures and the cell cycle arrest. Bad protein has been recognized as an important therapeutic target for various anti-glioma drugs and an ideal candidate for gene therapy.