Yeager T R, Neumann A A, Englezou A, Huschtscha L I, Noble J R, Reddel R R
Children's Medical Research Institute, Westmead, Sydney, New South Wales, Australia.
Cancer Res. 1999 Sep 1;59(17):4175-9.
Telomerase-negative immortalized human cells maintain their telomeres by a mechanism known as alternative lengthening of telomeres (ALT). We report here that ALT cells contain a novel promyelocytic leukemia (PML) body (ALT-associated PML body, APB). APBs are large donut-shaped nuclear structures containing PML protein, telomeric DNA, and the telomere binding proteins human telomere repeat binding factors 1 and 2. Immunostaining showed that APBs also contain replication factor A, RAD51, and RAD52, proteins involved in DNA synthesis and recombination. During immortalization, APBs appeared at exactly the same time as activation of ALT. APBs were found in ALT tumors and cell lines but not in mortal cell strains or in telomerase-positive cell lines or tumors.
端粒酶阴性的永生化人类细胞通过一种称为端粒替代延长(ALT)的机制来维持其端粒。我们在此报告,ALT细胞含有一种新型的早幼粒细胞白血病(PML)小体(ALT相关PML小体,APB)。APB是大型的甜甜圈状核结构,包含PML蛋白、端粒DNA以及端粒结合蛋白人类端粒重复结合因子1和2。免疫染色显示,APB还含有复制因子A、RAD51和RAD52,这些是参与DNA合成和重组的蛋白质。在永生化过程中,APB与ALT的激活同时出现。在ALT肿瘤和细胞系中发现了APB,但在正常细胞株、端粒酶阳性细胞系或肿瘤中未发现。