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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The human papillomavirus type 16 negative regulatory RNA element interacts with three proteins that act at different posttranscriptional levels
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The human papillomavirus type 16 negative regulatory RNA element interacts with three proteins that act at different posttranscriptional levels

机译：人类乳头瘤病毒16型负调控RNA元件与三种蛋白质的相互作用，这些蛋白质在转录后的水平不同

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摘要

In human papillomaviruses, expression of the late genes L1 and L2. encoding the capsid proteins, is restricted to the upper layers of the infected epithelium. A 79-nt GU-rich negative regulatory element (NRE) located at the 3' untranslated region of the human papilloma- virus 16 L1 gene was identified previously as key to the posttran- scriptional control of late gene expression. Here. we demonstrate that in epithelial cells, the NRE can directly bind the U2 auxiliary splicing factor 65-kDa subunit, the cleavage stimulation factor 64-kDa subunit, and the Elav-like HuR protein. On induction of epithelial cell differ- entiation, levels of the U2 auxiliary splicing factor 65-kDa subunit decrease, levels of the cleavage stimulation factor 64kDa subunit increase, and the levels of HuR remain unchanged. although redis- tribution of the HuR from the nucleus to the cytoplasm is observed. Late gene transcripts. which appear to be fully processed. are de- tected in undifferentiated W12 cells, but are confined in the nucleus. We propose that repression of late gene expression in basal epithelial cells may be caused by nuclear retention or cytoplasmic instability of NRE-containing late gene transcripts.
机译：在人乳头瘤病毒中，晚期基因L1和L2的表达。编码衣壳蛋白的编码被限制在被感染的上皮的上层。先前已鉴定出位于人乳头瘤病毒16 L1基因3'非翻译区的富含79 nt GU的负调控元件（NRE）是后期基因表达的转录后控制的关键。这里。我们证明，在上皮细胞中，NRE可以直接结合U2辅助剪接因子65-kDa亚基，裂解刺激因子64-kDa亚基和Elav-like HuR蛋白。诱导上皮细胞分化后，U2辅助剪接因子65-kDa亚基水平降低，切割刺激因子64kDa亚基水平升高，HuR水平保持不变。尽管观察到了HuR从细胞核到细胞质的重新分布。晚期基因转录物。似乎已完全处理。在未分化的W12细胞中被检测到，但被限制在细胞核中。我们建议阻遏晚基因表达在基底上皮细胞中可能是由含有NRE的晚基因转录物的核保留或细胞质不稳定性引起的。

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