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您的检索式：作者名="CHE YanChun"
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| 1 | Analysis of HSV-I ICP22 effects on HCMV major immediate-early promoter structure显示文摘The human cytomegalovirus (HCMV) major immediate-early (MIE) promoter has strong transcriptional promoting capability. Its cis-acting regulatory elements form a special structure in this region that is repeated multiple times; the biological significance of these elements and their different compositions in the transcriptional promoting process remain unclear. Our results demonstrate that the HSV-I MIE protein ICP22 can generate strong repression of many viral and cellular promoters and enhancers. We further studied the transcriptional effects of ICP22 on structural elements and mutations in various HCMV MIE promoters by using a CAT assay. In spite of different transcriptional effects of all the ele- ments in the presence of ICP22, the transcriptional efficiencies exhibited by mutations generated by different compositions and an entire HCMV promoter, are not the simple sum of the functions of these elements. Furthermore, the transcriptional activities of specific sequences were not affected by the presence of ICP22. Therefore, it is assumed that the HCMV MIE promoter co-regulates expression of downstream genes by using viral and cellular specific factors via a specific pathway. | LUO Jie, CUN Wei, CHE YanChun, WANG LiChun, LI WeiZhong, LIU LongDing & LI QiHan Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming 650118, China | 2007 | Science China(Life Sciences)2007，50，3： | 2 |
| 2 | A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5显示文摘Studies of herpes simplex virus type 1(HSV-1)infection have shown that many known and unknown cellular molecules involved in viral proliferation are up-regulated following HSV-1 infection.In this study,using two-dimensional polyacrylamide gel electrophoresis,we found that the expression of the HSV-1 infection response repressive protein(HIRRP,GI 16552881)was up-regulated in human L02 cells infected with HSV-1.HIRRP,an unknown protein,was initially localized in the cytoplasm and then translocated into the nucleus of HSV-1-infected cells.Further analysis showed that HIRRP represses HSV-1proliferation by inhibiting transcription of the viral genome by interacting with the cellular transcription factor,ATF5,via its N-terminal domain.ATF5 represses the transcription of many host genes but can also act as an activator of genes containing a specific motif.We found that ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection;HIRRP then induces feedback repression of this transcription by interacting with ATF5. | WU LianQiu ZHANG XueMei CHE YanChun ZHANG Ying TANG SongQing LIAO Yun NA RuiXiong XIONG XiangLin LIU LongDing LI QiHan | 2013 | Science China(Life Sciences)2013，56，12： | 2 |
| 3 | Egress of HSV-1 capsid requires the interaction of VP26 and a cellular tetraspanin membrane protein显示文摘 | Lei Wang Longding Liu Yanchun Che | | 0，，07： | 1 |
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