Xie An-Yong, Folk William R
Department of Biochemistry, University of Missouri-Columbia, Columbia, Missouri 65211, USA.
J Virol. 2002 Dec;76(23):11809-18. doi: 10.1128/jvi.76.23.11809-11818.2002.
When tethered in cis to DNA, the transcriptional corepressor mSin3B inhibits polyomavirus (Py) ori-dependent DNA replication in vivo. Histone deacetylases (HDACs) appear not to be involved, since tethering class I and class II HDACs in cis does not inhibit replication and treating the cells with trichostatin A does not specifically relieve inhibition by mSin3B. However, the mSin3B L59P mutation that impairs mSin3B interaction with N-CoR/SMRT abrogates inhibition of replication, suggesting the involvement of N-CoR/SMRT. Py large T antigen interacts with mSin3B, suggesting an HDAC-independent mechanism by which mSin3B inhibits DNA replication.
当转录共抑制因子mSin3B在顺式作用下与DNA相连时，它在体内抑制多瘤病毒（Py）ori依赖性DNA复制。组蛋白脱乙酰酶（HDAC）似乎不参与其中，因为在顺式作用下连接I类和II类HDAC不会抑制复制，用曲古抑菌素A处理细胞也不会特异性地解除mSin3B的抑制作用。然而，损害mSin3B与N-CoR/SMRT相互作用的mSin3B L59P突变消除了对复制的抑制作用，表明N-CoR/SMRT参与其中。Py大T抗原与mSin3B相互作用，提示mSin3B抑制DNA复制存在一种不依赖HDAC的机制。
