Protein encoded by HSV‐1 stimulation‐related gene 1 (HSRG1) interacts with and inhibits SV40 large T antigen

Guo, Huan; Wei, Cun; Liu, L. D.; Dong, Shuang; Wang, L. C.; Dong, Chuan; Li, Q. H.

doi:10.1111/j.1365-2184.2006.00408.x

Cited by 7 publications

(8 citation statements)

References 39 publications

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“…As a member of the SAND family, it is important to understand the functions of HSRG1. We previously found that HSRG1 specifically interacts with amino acids 132-450 of the SV40 large T antigen, and that transcriptional activity of SV40 promoters activated by large T was inhibited by HSRG1 [10]. We suggested that HSRG1 might have a role in cellular transcriptional regulation.…”

Section: Discussionmentioning

confidence: 90%

“…Proteins induced by viral infection have been intensively studied [6,7,10] and the functions of these proteins have been gradually clarified. HSRG1, belonging to the conserved SAND protein family, is one of the proteins upregulated in early stages of HSV-1 infection.…”

Section: Discussionmentioning

confidence: 99%

“…HSRG1 is expressed 2 h after infection and is classified as a SAND protein family member [8], containing a eukaryotic conserved domain [9] of unknown biological function. Our earlier work also indicated that HSRG1 interacts with the SV40 large T-antigen (LT), altering transcriptional regulation of LT from the SV40 promoter [10]. These results suggested that HSRG1 could interact with transcriptional regulatory proteins.…”

mentioning

confidence: 86%

“…The gene encoding Cyclin T2 was obtained by PCR amplification with primers CycT2a-F1 and CycT2a-R1 (Table 1). Eukaryotic expression plasmid pcDNA3-HSRG1, expressing HSRG1, has already been constructed in our laboratory [10]. Recombination plasmid pGADT7-HSRG1 was constructed by ligating the HSRG1 gene (amplified with primers HSRG1-F1 and HSRG1-R1) into the pGADT7 vector (Clontech).…”

Section: Plasmid Constructionmentioning

confidence: 99%

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HSV-1 stimulation-related protein HSRG1 inhibits viral gene transcriptional elongation by interacting with Cyclin T2

et al. 2011

Sci. China Life Sci.

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The protein encoded by HSRG1 (HSV-1 stimulation-related gene 1) is a virally induced protein expressed in HSV-1-infected cells. We have already reported that HSRG1 is capable of interacting with transcriptional regulator proteins. To further analyze the effects of HSRG1 on the regulation of viral gene transcription, we expressed the HSRG1 protein in transfected cells and found that it postpones the proliferation of HSV-1. CAT (chloramphenicol acetyltransferase) assays also revealed that HSRG1 reduces transcription from HSV-1 promoters. Yeast two-hybrid and immunoprecipitation assays indicated that HSRG1 interacts with Cyclin T2, the regulatory subunit of P-TEFb, which is required for transcription elongation by RNA Pol II (RNAP II), and that amino acid residues 1-420 in Cyclin T2 are important for binding with HSRG1. Fluorescence assays suggested that the cellular localizations of those two proteins are influenced by their interaction. Further analyses with CAT assays revealed that HSRG1 inhibits the transcriptional activation by Cyclin T2 of viral promoters. Our results suggested that the inhibitory effects of HSRG1 on viral replication and proliferation are probably induced by its binding to Cyclin T2. Therefore, it is likely that HSRG1 inhibits viral gene transcriptional elongation by interacting with Cyclin T2.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 86%

Section: Plasmid Constructionmentioning

confidence: 99%

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HSV-1 stimulation-related protein HSRG1 inhibits viral gene transcriptional elongation by interacting with Cyclin T2

et al. 2011

Sci. China Life Sci.

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“…T抗原产生相互作用, 并影响大T抗原对SV40 启动子的转录起始功能 [10] , 该结果提示 HSRG1 具有与转录调控蛋白相互作用的特性. 因此, 进一步利用酵母双杂交技术研究了该蛋白分子在细胞内可能的作用蛋白.…”

Section: 析发现它能与猴病毒Sv40 的重要转录调控蛋白大unclassified

HSV-1病毒感染细胞诱导蛋白hsrg1影响病毒基因转录的延伸

吴¹,

李²,

余³

et al. 2010

Sci. Sin.-Vitae

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A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5

Zhang

Che

et al. 2013

Sci. China Life Sci.

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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-1 proliferation 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.

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Protein encoded by HSV‐1 stimulation‐related gene 1 (HSRG1) interacts with and inhibits SV40 large T antigen

Cited by 7 publications

References 39 publications

HSV-1 stimulation-related protein HSRG1 inhibits viral gene transcriptional elongation by interacting with Cyclin T2

HSV-1 stimulation-related protein HSRG1 inhibits viral gene transcriptional elongation by interacting with Cyclin T2

HSV-1病毒感染细胞诱导蛋白hsrg1影响病毒基因转录的延伸

A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5

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