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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Position-dependent activity of α-fetoprotein enhancer element Ⅲ in the adult liver is due to negative regulation
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Position-dependent activity of α-fetoprotein enhancer element Ⅲ in the adult liver is due to negative regulation

机译：成年肝脏中甲胎蛋白增强子元素Ⅲ的位置依赖性活性是由于负调控

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摘要

α-Fetoprotein (AFP) transcription is activated early in hepatogen- esis, but is dramatically repressed within several weeks after birth. AFP regulation is governed by multiple elements including three enhancers termed EⅠ, EⅡ, and EⅢ. All three AFP enhancers continue to be attive in the adult liver, where EⅠ and EⅡ exhibit high levels of activity in pericentral hepatocytes with a gradual reduction in activity in a pericentral-periportal direction. In contrast to these two enhancers, EⅢ activity is highly restricted to a layer of cells surrounding the central veins. To test models that could account for position-dependent EⅢ activity in the adult liver, we have analyzed transgenes in which AFP enhancers EⅡ and EⅢ were linked together. Our results indicate that the activity of EⅢ is dominant over that of EⅡ, indicating that EⅢ is a potent negative regulatory element in all hepatocytes except those encircling the central veins. We have localized this negative activity to a 340-bp fragment. This suggests that enhancer Ⅲ may be involved in postnatal AFP repression.
机译：α-甲胎蛋白（AFP）转录在肝细胞生成早期被激活，但在出生后数周内被显着抑制。 AFP调节受多种因素控制，包括三种增强剂，分别称为EⅠ，EⅡ和EⅢ。这三种AFP增强剂在成年肝脏中仍保持着活性，其中EⅠ和EⅡ在中枢肝细胞中显示出高水平的活性，并在中枢周周方向上逐渐降低活性。与这两种增强剂相比，EⅢ活性高度受限于中央静脉周围的一层细胞。为了测试可以解释成年肝脏中位置依赖的EⅢ活性的模型，我们分析了AFP增强子EⅡ和EⅢ连接在一起的转基因。我们的研究结果表明，EⅢ的活性高于EⅡ，表明EⅢ是除环绕中央静脉的所有肝细胞中有效的负调控元件。我们已经将该负活性定位为一个340 bp的片段。这表明增强子Ⅲ可能参与了出生后AFP的抑制。

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