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作 者:Yujing Huang Xin Guo Jing Zhang Jianming Li Mingyi Xu Qing Wang Zhongyang Liu Yanping Ma Ying Qi Qiang Ruan
机构地区:[1]Virology Laboratory,Shengjing Hospital of China Medical University,Shenyang,110004,China [2]Department of Pediatrics,Shengjing Hospital of China Medical University,Shenyang,110004,China [3]Department of Obstetrics and Gynecology,Shengjing Hospital of China Medical University,Shenyang,110004,China [4]Department of Pediatrics,The Fourth Affiliated Hospital,China Medical University,Shenyang,110033,China
出 处:《Virologica Sinica》2022年第3期358-369,共12页中国病毒学(英文版)
基 金:supported by the National Natural Science Foundation of China(82071664)。
摘 要:Human cytomegalovirus(HCMV)is a ubiquitous pathogen belongs to betaherpesvirus subfamily.RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20%of total viral transcripts.In our study,functions of HCMV RNA2.7 were investigated by comparison of host cellular transcriptomes between cells infected with HCMV clinical strain and RNA2.7 deleted mutant.It was demonstrated that RNA polymeraseⅡ(PolⅡ)-dependent host gene transcriptions were significantly activated when RNA2.7 was removed during infection.A145 nt-in-length motif within RNA2.7 was identified to inhibit the phosphorylation of PolⅡSerine-2(PolⅡS2)by reducing the interaction between PolⅡand phosphorylated cyclin-dependent kinase 9(pCDK9).Due to the loss of PolⅡS2 phosphorylation,cellular DNA pre-replication complex(pre-RC)factors,including Cdt1 and Cdc6,were significantly decreased,which prevented more cells from entering into S phase and facilitated viral DNA replication.Our results provide new insights of HCMV RNA2.7 functions in regulation of host cellular transcription.
关 键 词:Human cytomegalovirus(HCMV) RNA2.7 RNA polymeraseⅡ(PolⅡ) Cyclin-dependent kinase 9(CDK9) PHOSPHORYLATION
分 类 号:R373[医药卫生—病原生物学]
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