Araki K, Miyazaki J, Tsurimoto T, Inomoto T, Iwanaga T, Matsubara K, Yamamura K
Institute for Medical Genetics, Kumamoto University Medical School.
Jpn J Cancer Res. 1989 Apr;80(4):295-8. doi: 10.1111/j.1349-7006.1989.tb02308.x.
In 14p3HB transgenic mice, which carry three tandem copies of hepatitis B virus (HBV) DNA, the HBV DNA was significantly methylated and no viral proteins were produced. To analyze the causal relationship between hypermethylation and gene inactivity, 5-azacytidine was injected into the mice to demethylate HBV DNA. When postnatal 14p3HB mice were treated with the drug, hepatitis virus surface antigen was produced in these mice by 3 weeks of age, and the integrated HBV DNA of the liver was less heavily methylated. Our results suggest that injection of 5-azacytidine can be used to efficiently activate a silent transgene such as HBV DNA in transgenic mice.
在携带三个串联拷贝乙肝病毒(HBV)DNA的14p3HB转基因小鼠中,HBV DNA发生了显著甲基化,且未产生病毒蛋白。为分析高甲基化与基因失活之间的因果关系,向小鼠注射5-氮杂胞苷以使HBV DNA去甲基化。当对出生后的14p3HB小鼠进行药物处理时,这些小鼠在3周龄时产生了肝炎病毒表面抗原,且肝脏中整合的HBV DNA甲基化程度降低。我们的结果表明,注射5-氮杂胞苷可用于有效激活转基因小鼠中如HBV DNA这样的沉默转基因。