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| 1 | The Herpes Simplex Virus Type 1 Infected Cell Protein 22显示文摘As one of the immediate-early(IE)proteins of herpes simplex virus type 1(HSV-1),ICP22 is a multifunctional viral regulator that localizes in the nucleus of infected cells.It is required in experimental animal systems and some nonhuman cell lines,but not in Vero or HEp-2 cells.ICP22 is extensively phosphorylated by viral and cellular kinases and nucleotidylylated by casein kinase Ⅱ.It has been shown to be required for efficient expression of early(E)genes and a subset of late(L)genes.ICP22,in conjunction with the UL13 kinase,mediates the phosphorylation of RNA polymerase Ⅱ.Both ICP22 and UL13 are required for the activation of cdc2,the degradation of cyclins A and B and the acquisition of a new cdc2 partner,the UL42 DNA polymerase processivity factor.The cdc2-UL42 complex mediates postranscriptional modification of topoisomerase Ⅱα in an ICP22-dependent manner to promote L gene expression.In addition,ICP22 interacts with cdk9 in a Us3 kinase dependent fashion to phosphorylate RNA polymerase Ⅱ. | Alan C.ZHENG | 2010 | Virologica Sinica2010，25，1： | 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 | Zr基非晶合金与铜的扩散连接研究(英文)显示文摘利用Gleeble 3500热模拟试验机在添加和未添加扩散连接中间层条件下对Zr_(41.25)Ti_(13.75)Cu_(12.5)Ni_(10)Be_(22.5)块体非晶合金与纯铜的扩散连接性进行了研究。实验结果表明,在2种条件下均获得了无裂纹和空洞的良好的连接界面。通过能谱分析和电子探针分析,在连接界面处观察到明显的原子扩散,但原子扩散距离较窄。非晶合金中晶化相的出现促进了界面处原子的扩散。 | 寇宏超 管恒 王军 唐斌 李金山 | 2016 | 稀有金属材料与工程2016，45，1： | 1 |
| 4 | 利用IE基因表达外源抗原的HSVⅠ重组病毒的构建显示文摘目的 研究ICP22蛋白缺失是否影响病毒的感染复制以及ICP22蛋白在病毒水平上功能.方法 利用同源重组方法用绿色荧光蛋白(green fluorescent protein,GFP)的编码基因取代ICP22蛋白的编码基因,以流式细胞仪分选结合蚀斑筛选的方法得到ICP22蛋白缺失的单克隆重组病毒.结果 对ICP22蛋白缺失重组病毒进行绿色荧光的表达情况的镜下观察、GFP基因序列的测定、重组病毒中GFP基因的定量PCR检测、GFP蛋白表达的Western 印迹 检测等方法进行了验证,成功构建了ICP22蛋白缺失的重组病毒,并在研究过程中发现ICP22蛋白缺失的重组病毒出现感染复制停滞的现象.结论 ICP22蛋白缺失的重组病毒出现感染复制停滞的现象提示其在细胞中具有重要的功能. | 崔伟 刘龙丁 张莹 王蕾 廖芸 王晶晶 郭磊 赵红玲 王丽春 董承红 李琦涵 | 2011 | 医学分子生物学杂志2011，8，3： | 0 |
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