BRCA1 interaction with RNA polymerase II reveals a role for hRPB2 and hRPB10alpha in activated transcription.
BRCA1 interaction with RNA polymerase II reveals a role for hRPB2 and hRPB10alpha in activated transcription.
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BRCA1 与 RNA 聚合酶 II 的相互作用揭示了 hRPB2 和 hRPB10α 在激活转录中的作用。
DOI：
10.1073/pnas.97.7.3148
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发表时间：
2000
影响因子：
11.1
通讯作者：
Parvin,JD
中科院分区：
文献类型：
--
作者：
Schlegel,BP;Green,VJ;Ladias,JA;Parvin,JD
RNA聚合酶II(POL II)酶的12个亚基中的大部分功能尚不清楚。在这项研究中，我们证明了其中两个亚基，hRPB2和hRPB10α，介导了转录的调节刺激。我们发现转录共激活子BRCA1在体外直接与核心POL II复合体相互作用。我们测试了Pol II的单亚基是否会与完整的Pol II复合体竞争，以抑制BRCA1刺激的转录。过量纯化的POLII亚基hRPB2或hRPB10α在体外阻断了依赖于BRCA1和VP16的转录激活，而对基础转录的影响很小。在这些检测中，没有其他Pol II亚基抑制激活的转录。此外，hRPB10α，而不是hRPB2，阻断了Sp1依赖的激活。
The functions of most of the 12 subunits of the RNA polymerase II (Pol II) enzyme are unknown. In this study, we demonstrate that two of the subunits, hRPB2 and hRPB10α, mediate the regulated stimulation of transcription. We find that the transcriptional coactivator BRCA1 interacts directly with the core Pol II complexin vitro. We tested whether single subunits from Pol II would compete with the intact Pol II complex to inhibit transcription stimulated by BRCA1. Excess purified Pol II subunits hRPB2 or hRPB10α blocked BRCA1- and VP16-dependent transcriptional activationin vitrowith minimal effect on basal transcription. No other Pol II subunits tested inhibited activated transcription in these assays. Furthermore, hRPB10α, but not hRPB2, blocked Sp1-dependent activation.