Expression data from Hela cells stably expressing the wild-type preS and the three mutant preS
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ABSTRACT: In large cohort studies, several preS mutants were identified as independent risk factors for HCC risk.In order to study the carcinogenic mechanism between different mutants, HeLa cell lines expressing wild type and different mutated preS proteins were constructed. We used microarrays to describe gene expression in HeLa cells stably expressing the wild-type preS and the three mutant preS, and to identify distinct classes of up-regulated genes.
Project description:In large cohort studies, several HBx mutants were identified as independent risk factors for HCC risk.In order to study the carcinogenic mechanism between different mutants, HeLa cell lines expressing wild type and different mutated HBx proteins were constructed. We used microarrays to describe gene expression in HeLa cells stably expressing the wild-type HBx and the four mutant HBx, and to identify distinct classes of up-regulated genes.
Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes.
Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes. UHRF1 was depleted in HeLa cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-related genes expression profiles were compared among control cells, UHRF1-depleted cells, UHRF1 WT reconstituting cells and UHRF1 S674A mutant reconstituting cells.
Project description:The oncolytic potential of NDV has gained significant attention in the context of clinical trials. After systematically comparing the oncolytic activities of different NDV subtypes,we found that all subtypes, except for highly pathogenic genotype VII NDVs, display remarkable infectivity on tumor cell lines.A single amino acid mutation (F450L) in the NP protein at position 450 leads to an approximate 1000000-fold increase in the TCID50 value of genotype VII NDVs on tumor cells.Mechanistic inquiries unveiled that the amino acid at position 450 of the NP protein governs preferential translation of NDV mRNA.The preferential translation that regulates viral mRNA translation is often accompanied by modulation of the host translation machinery. Therefore, we established HeLa cell lines stably expressing NP protein from different NDV strains. Ribosome-bound mRNA was enriched to perform Ribosome Nascent-chain Complex sequencing(RNC-seq), while total cellular mRNA was enriched to conducted RNA-Seq . Untreated cells were used as controls. These experiments aimed to investigate the impact of NP on the host translation system.
Project description:We have found that exogenous expression of matrin 3 in chicken DT40 cells and human HeLa cells suppressed expression of endogenous matrin 3 at mRNA level. To find other genes showing decreased expression by exogenous matrin 3, gene expression profiles of wild-type HeLa cells and HeLa cells expressing GFP-tagged chicken matrin 3 were compared.
Project description:Cx32 wildtype and mutants (W3S, R22G) were expressed in HeLa cells and subjected to surface biotinylation to check for expression level differences between the different conditions. A CFP control was conducted.