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作 者:YU Xian1,2, LI WeiZhong1, LIU LongDing1, CHE YanChun1, CUN Wei1, WU WenJuan1, HE ChunYan1, SHAO CongWen1 & LI QiHan1 1 Department of Viral Immunology, Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming 650118, China 2 Institute of Materia Medica, North Sichuan Medical College, Nanchong 637007, China
出 处:《Science China(Life Sciences)》2008年第11期966-972,共7页中国科学(生命科学英文版)
基 金:the National Natural Science Foundation of China (Grant Nos. 30570081,30670094 and 30700028)
摘 要:The herpes simplex virus type 1 (HSV-1) tegument proteins have important functions in the viral repli- cation process. In order to investigate the role of the HSV-1 tegument protein VP22 in viral replication, its transcriptional regulation of viral promoters was investigated using the chloramphenicol acetyl- transferase (CAT) assay. The results indicate that VP22 exerts a dose-dependent transcriptional in- hibitory effect on the HSV-1 α4, TK, and gC gene promoters. VP22 had the capacity to repress tran- scriptional activation of promoters via different viral transcription regulatory factors such as VP16 and ICP0, as evidenced by the specific repression of the TK and gC gene promoters by ICP0. In addition, VP22 was capable of inhibiting the promotion of ICP0 transcriptional activation in the presence of HAT PCAF, which is even more remarkable than the VP22 repression of ICP0 transcriptional activation. Fi- nally, the transcriptional inhibitory effect of VP22 on other viral promoters was demonstrated by the analysis of β-galactosidase activities in internal controls.The herpes simplex virus type 1 (HSV-1) tegument proteins have important functions in the viral repli- cation process. In order to investigate the role of the HSV-1 tegument protein VP22 in viral replication, its transcriptional regulation of viral promoters was investigated using the chloramphenicol acetyl- transferase (CAT) assay. The results indicate that VP22 exerts a dose-dependent transcriptional in- hibitory effect on the HSV-1 α4, TK, and gC gene promoters. VP22 had the capacity to repress tran- scriptional activation of promoters via different viral transcription regulatory factors such as VP16 and ICP0, as evidenced by the specific repression of the TK and gC gene promoters by ICP0. In addition, VP22 was capable of inhibiting the promotion of ICP0 transcriptional activation in the presence of HAT PCAF, which is even more remarkable than the VP22 repression of ICP0 transcriptional activation. Fi- nally, the transcriptional inhibitory effect of VP22 on other viral promoters was demonstrated by the analysis of β-galactosidase activities in internal controls.
关 键 词:HERPES SIMPLEX virus type 1 TEGUMENT VP22 TRANSCRIPTIONAL regulation
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