端粒酶
端粒
早幼粒细胞白血病蛋白
生物
细胞培养
免疫染色
癌症研究
DNA
分子生物学
雷达51
白血病
急性早幼粒细胞白血病
突变
永生化细胞系
细胞生物学
同源重组
遗传学
免疫学
免疫组织化学
基因
维甲酸
作者
Thomas R. Yeager,Axel A. Neumann,Anna Englezou,Lily I. Huschtscha,Jane R. Noble,Roger R. Reddel
出处
期刊:PubMed
[National Institutes of Health]
日期:1999-09-01
卷期号:59 (17): 4175-9
被引量:691
摘要
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.
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