Recent studies have suggested that wild-type p53 blocks cell cycle progression near the G1-S boundary and is involved in both differentiation and apoptosis in many types of cells including cancer cells. p53 expression is enhanced upon DNA-damaging apoptotic stimuli while Fas/Apo-1, a member of the tumor necrosis factor receptor family expressed on cell surface, transduces a signal for apoptosis upon specific ligand or antibody engagement. We demonstrated that stable transfection of the wild-type p53 gene under the control of CMV promoter induced differentiation and apoptosis under restricted conditions in cancer cells, and often caused sensitization of p53-transfected cells to Fas/Apo-1 signal. To investigate the interaction between two major apoptotic pathways involving p53 and Fas/Apo-1 we have established a system that allows to induce wild-type p53 overexpression and apoptosis in cancer cells upon treatment with anti-Fas antibody. The system also allows to investigate other factors interacting with p53 and Fas/Apo-1, and should provide a clue to understanding the biological and biochemical aspects of apoptosis.

译文

最近的研究表明,野生型p53阻断G1-S边界附近的细胞周期进程,并参与包括癌细胞在内的许多类型细胞的分化和凋亡。p53表达在破坏DNA的凋亡刺激时增强,而Fas/Apo-1 (在细胞表面表达的肿瘤坏死因子受体家族的成员) 在特异性配体或抗体接合时转导凋亡信号。我们证明,在CMV启动子控制下,野生型p53基因的稳定转染可在限制条件下诱导癌细胞的分化和凋亡,并经常引起p53-transfected细胞对Fas/Apo-1信号的敏感性。为了研究涉及p53和Fas/Apo-1的两个主要凋亡途径之间的相互作用,我们建立了一个系统,该系统允许在用抗Fas抗体治疗后诱导野生型p53过表达和癌细胞凋亡。该系统还允许研究与p53和Fas/Apo-1相互作用的其他因素,并且应该为了解凋亡的生物学和生化方面提供线索。

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