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Gene Expression Profiles of HeLa Cells Impacted by Hepatitis C Virus Non-structural Protein NS4B
( Yi Zheng ),( Lin Bai Ye ),( Jing Liu ),( Wei Jing ),( Khalid A. Timani ),( Xiao Jun Yang ),( Fan Yang ),( Wei Wang ),( Bo Gao ),( Zhen Hui Wu ) 생화학분자생물학회 2005 BMB Reports Vol.38 No.2
By a cDNA array representing 2308 signal transductionrelated genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT PCR; and the aldo-keto reductase family 1, member Cl (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.
Fang, Xiaonan,Ye, Lin-Bai,Zhang, Yijuan,Li, Baozong,Li, Shanshan,Kong, Lingbao,Wang, Yuhua,Zheng, Hong,Wang, Wei,Wu, Zhenghui The Microbiological Society of Korea 2006 The journal of microbiology Vol.44 No.5
GST pull-down assays were used to characterize the SARS-CoV membrane (M) and nucleocapsid (N) interaction, and it was found that the amino acids 211-254 of N protein were essential for this interaction. When tetrad glutamines (Q) were replaced with glutamic acids (E) at positions of 240-243 of the N protein, the interaction was disrupted.
Xiaonan Fang,Lin-Bai Ye,Yijuan Zhang,Baozong Li,Shanshan Li,Lingbao Kong,Yuhua Wang,Hong Zheng,Wei Wang,Zhenghui Wu 한국미생물학회 2006 The journal of microbiology Vol.44 No.5
GST pull-down assays were used to characterize the SARS-CoV membrane (M) and nucleocapsid (N)interaction, and it was found that the amino acids 211-254 of N protein were essential for this interaction. When tetrad glutamines (Q) were replaced with glutamic acids (E) at positions of 240-243 of the N protein, the interaction was disrupted.
Gene Expression Profiles of HeLa Cells Impacted by Hepatitis C Virus Non-structural Protein NS4B
Zheng, Yi,Ye, Lin-Bai,Liu, Jing,Jing, Wei,Timani, Khalid A.,Yang, Xiao-Jun,Yang, Fan,Wang, Wei,Gao, Bo,Wu, Zhen-Hui Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.2
By a cDNA array representing 2308 signal transduction related genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT-PCR; and the aldo-keto reductase family 1, member C1 (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.
( Xing Ming Ye ),( Wen Dong Bai ),( Hua Yu Zhu ),( Xiao Zhang ),( Ying Chen ),( Lei Wang ),( An Gang Yang ),( Jing Zh Ao ),( Lin Tao Jia ) 생화학분자생물학회 2014 BMB Reports Vol.47 No.5
HER2-overexpressing breast cancers are characterized byfrequent distant metastasis and often develop resistance aftershort-term effective treatment with the monoclonal antibodydrug, trastuzumab. Here, we found that the oncogenic miRNA,miR-221, inhibited apoptosis, induced trastuzumab resistanceand promoted metastasis of HER2-positive breast cancers. Thetumor suppressor PTEN was identified as a miR-221 target;overexpression of PTEN abrogated the aforementionedmiR-221-induced malignant phenotypes of the cells. Thesefindings indicate that miR-221 may promote trastuzumabresistance and metastasis of HER2-positive breast cancers bytargeting PTEN, suggesting its role as a potential biomarker forprogression and poor prognosis, and as a novel target fortrastuzumab-combined treatment of breast cancers.[BMB Reports 2014; 47(5): 268-273]