Human papillomaviruses (HPV) such as HPV16 and HPV31 encode an E8^E2 protein that acts as a repressor of viral replication and transcription. E8^E2′s repression activities are mediated via the interaction with host-cell NCoR (nuclear receptor corepressor)/SMRT (silencing mediator of retinoid and thyroid receptors) corepressor complexes, which consist of NCoR, its homologue SMRT, GPS2 (G-protein pathway suppressor 2), HDAC3 (histone deacetylase 3), TBL1 (transducin b-like protein 1) and its homologue TBLR1 (TBL1-related protein 1). We now provide evidence that transcriptional repression by HPV31 E8^E2 is NCoR/SMRT-dependent but surprisingly always HDAC3-independent when analysing different HPV promoters. This is in contrast to the majority of several cellular transcription factors using NCoR/SMRT complexes whose transcriptional repression activities are both NCoR/SMRT- and HDAC3-dependent. However, NCoR/SMRT-dependent but HDAC3-independent repression has been described for specific cellular genes, suggesting that this may not be specific for HPV promoters but could be a feature of a subset of NCoR/SMRT-HDAC3 regulated genes.

中文翻译：

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HDAC3对人乳头瘤病毒31 E8 ^ E2蛋白的转录抑制的贡献。

人乳头瘤病毒（HPV）（例如HPV16和HPV31）编码一种E8 ^ E2蛋白，可作为病毒复制和转录的阻遏物。E8 ^ E2的抑制活性是通过与宿主细胞NCoR（核受体共抑制物）/ SMRT（类维生素A和甲状腺受体的沉默介导物）共抑制物复合物相互作用而介导的，复合物由NCoR，其同源SMRT，GPS2（G蛋白）组成。通路抑制剂2），HDAC3（组蛋白脱乙酰基酶3），TBL1（转导蛋白b样蛋白1）及其同系物TBLR1（TBL1相关蛋白1）。我们现在提供证据，当分析不同的HPV启动子时，HPV31 E8 ^ E2的转录抑制是NCoR / SMRT依赖性的，但令人惊讶的是总是HDAC3依赖性的。这与大多数使用NCoR / SMRT复合物的细胞转录因子相反，后者的转录抑制活性均依赖于NCoR / SMRT和HDAC3。但是，已经描述了对特定细胞基因的NCoR / SMRT依赖性但非HDAC3依赖性阻遏，提示这可能对HPV启动子不是特异性的，但可能是NCoR / SMRT-HDAC3调控基因的一个子集。