转录因子Oct1与猿猴病毒40复制起点的富含AT的片段结合。
Transcription factor Oct1 binds to the AT-rich segment of the simian virus 40 replication origin.
作者信息
Kilwinski J, Baack M, Heiland S, Knippers R
机构信息
Division of Biology, Universität Konstanz, Federal Republic of Germany.
出版信息
J Virol. 1995 Jan;69(1):575-8. doi: 10.1128/JVI.69.1.575-578.1995.
Abstract
A cellular protein that binds to the AT-rich late segment of the simian virus 40 (SV40) origin of replication has been identified as transcription factor Oct1. This conclusion is based on the following observations: the late origin binding protein has a molecular mass of about 100 kDa, like factor Oct1, and shares other biochemical properties with Oct1; its binding to the origin is inhibited by antibodies directed against the POU domain of factor Oct1; the isolated POU domain of Oct1 specifically binds to the SV40 late origin region. Thus, the SV40 genome contains binding sites for transcription factor Oct1 in the origin of replication in addition to the previously characterized octamer sites in the viral promoter enhancer. Oct1, bound to the viral origin, negatively affects the DNA unwinding reaction catalyzed by the viral replication initiator T antigen, suggesting that Oct1 may have a role in the regulation of viral replication.
摘要
一种与猿猴病毒40（SV40）复制起点富含AT的晚期片段结合的细胞蛋白已被鉴定为转录因子Oct1。这一结论基于以下观察结果：晚期起点结合蛋白的分子量约为100 kDa，与Oct1因子相同，并且与Oct1具有其他生化特性；其与起点的结合受到针对Oct1因子POU结构域的抗体的抑制；Oct1的分离POU结构域特异性结合SV40晚期起点区域。因此，除了病毒启动子增强子中先前已鉴定的八聚体位点外，SV40基因组在复制起点还含有转录因子Oct1的结合位点。与病毒起点结合的Oct1对病毒复制起始因子T抗原催化的DNA解旋反应产生负面影响，这表明Oct1可能在病毒复制调控中发挥作用。
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