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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Epstein-Barr nuclear antigen leader protein coactivates transcription through interaction with histone deacetylase 4
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Epstein-Barr nuclear antigen leader protein coactivates transcription through interaction with histone deacetylase 4

机译：爱泼斯坦-巴尔核抗原前导蛋白通过与组蛋白脱乙酰基酶4的相互作用共同激活转录

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摘要

Epstein-Barr nuclear antigen (EBNA) leader protein (EBNALP) co-activates promoters with EBNA2 and is important for Epstein-Barr virus immortalization of B cells. Investigation of the role of histone cleacetylases (HDACs) in EBNALP and EBNA2 promoter regulation has now identified EBNALP and EBNA2 to be associated with HIDAC4 in a lymphoblastoid cell line. Furthermore, a transcription-deficient EBNALP point mutant did not associate with HDAC4. HIDAC4 and 5 overexpression repressed EBNA2 activation and EBNALP coactivation, whereas other HDACs had little effect. Moreover, EBNALP expression decreased nuclear HDAC4. Expression of 14-3-3 anchors HDAC4 in the cytoplasm, increased EBNALP effects, and reversed HDAC4 or 5 repression. HIDAC4 reversal depended on the HDAC4 nuclear export sequence. Consistent with EBNALP coactivation being mediated by nuclear HIDAC4 depletion, HIDAC4 overexpression increased nuclear HIDAC4 and specifically repressed EBNA2-dependent activation as well as EBNALP-dependent coactivation. Also, EBNALP, HDAC4, and 14-3-3 could be immunoprecipitated in a single complex. Thus, these data strongly support a model in which EBNALP coactivates transcription by relocalizing HIDAC4 and 5 from EBNA2 activated promoters to the cytoplasm. The observed EBNALP effects are likely also in part through HIDAC5, which is highly homologous to HIDAC4.
机译：爱泼斯坦-巴尔核抗原（EBNA）前导蛋白（EBNALP）与EBNA2共激活启动子，对于E斯坦-巴尔病毒使B细胞永生化非常重要。对组蛋白乙酰化酶（HDAC）在EBNALP和EBNA2启动子调控中的作用的研究现已确定，EBNALP和EBNA2与成淋巴细胞样细胞系中的HIDAC4相关。此外，转录缺陷的EBNALP点突变体与HDAC4不相关。 HIDAC4和5过表达抑制EBNA2激活和EBNALP共激活，而其他HDAC几乎没有影响。此外，EBNALP表达降低了核HDAC4。 14-3-3的表达在细胞质中锚定了HDAC4，增加了EBNALP的作用，并逆转了HDAC4或5的阻遏作用。 HIDAC4逆转取决于HDAC4核输出序列。与核HIDAC4耗竭介导的EBNALP共激活一致，HIDAC4过表达增加了核HIDAC4的表达，并特别抑制了EBNA2依赖性激活以及EBNALP依赖性共激活。同样，EBNALP，HDAC4和14-3-3可在单个复合物中免疫沉淀。因此，这些数据强烈支持其中EBNALP通过将HIDAC4和5从EBNA2激活的启动子重新定位到细胞质来共激活转录的模型。观察到的EBNALP效应也可能部分是通过与HIDAC4高度同源的HIDAC5引起的。

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