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Temporal order of chromatin structural changes associated with activation of the major chicken vitellogenin gene.与鸡主要卵黄蛋白原基因激活相关的染色质结构变化的时间顺序。
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In contrast to other Xenopus genes the estrogen-inducible vitellogenin genes are expressed when totally methylated.与其他非洲爪蟾基因不同，雌激素诱导的卵黄蛋白原基因在完全甲基化时仍会表达。
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5-氮杂胞苷引起的去甲基化作用导致转基因小鼠中乙型肝炎病毒表面抗原的表达。

Demethylation by 5-azacytidine results in the expression of hepatitis B virus surface antigen in transgenic mice.

作者信息

Araki K, Miyazaki J, Tsurimoto T, Inomoto T, Iwanaga T, Matsubara K, Yamamura K

机构信息

Institute for Medical Genetics, Kumamoto University Medical School.

出版信息

Jpn J Cancer Res. 1989 Apr;80(4):295-8. doi: 10.1111/j.1349-7006.1989.tb02308.x.

DOI:10.1111/j.1349-7006.1989.tb02308.x
PMID:2473052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5917734/
Abstract

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.

摘要

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。