Scarr Rebecca B, Sharp Phillip A
Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts, MA 02139-4307, USA.
Oncogene. 2002 Aug 8;21(34):5245-54. doi: 10.1038/sj.onc.1205647.
Temperature sensitive mutations in host cell factor 1 (HCF-1) arrest cells in the middle of the G1 phase of the cycle. We have shown that the highly conserved C-terminal WYF domain of HCF-1 protein interacts with the MYND domain of the PDCD2 protein. This inter-action is conserved between human HCF-1 and HCF-2 and the C. elegans HCF. Overexpression of PDCD2, which interacts with the N-CoR/mSin3A corepressor complexes, suppresses cotransfected HCF-1 complement-ation of a temperature lesion in the endogenous HCF-1 protein. Overexpression of domains of either PDCD2 or HCF-1, which should interfere with interactions between these two proteins, enhances the complementation.
宿主细胞因子1（HCF-1）中的温度敏感突变会使细胞停滞在细胞周期的G1期中期。我们已经表明，HCF-1蛋白高度保守的C端WYF结构域与PDCD2蛋白的MYND结构域相互作用。这种相互作用在人类HCF-1和HCF-2以及秀丽隐杆线虫HCF之间是保守的。与N-CoR/mSin3A共抑制复合物相互作用的PDCD2的过表达会抑制内源性HCF-1蛋白中温度损伤的共转染HCF-1互补作用。PDCD2或HCF-1结构域的过表达会干扰这两种蛋白之间的相互作用，从而增强互补作用。
