ABSTRACT: Perform CUT-Tag analysis by H3K4m2 antibodies to investigate the role of H3K4 methylation in control Ramos cells (Ramos), the lentivirus vector infected Ramos cells (Ramos-Lv-Vector) and Ramos-Lv-ZEBRA.
Project description:Perform CHIP-seq analysis by H3K9m2 antibodies to investigate the role of H3K9 methylation in control Ramos cells (Ramos), the lentivirus vector infected Ramos cells (Ramos-Lv-Vector) and Ramos-Lv-ZEBRA.
| PRJNA1067391 | ENA
Project description:Perform CHIP-seq analysis by Pax5 antibodies to investigate the changes in Pax5 transcriptional regulation between control Ramos cells (Ramos), the lentivirus vector infected Ramos cells (Ramos-Lv-Vector) and Ramos-Lv-ZEBRA.
Project description:EBV immediate early protein ZEBRA was corroborated to interact with Pax5 which controls the fate of B cells. Ramos cells were infected with ZEBRA-expression lentivirus and positively infected cells were sorted, which were named Ramos-Lv-ZEBRA.
Project description:EBV immediate early protein ZEBRA was corroborated to interact with Pax5 which controls the fate of B cells. Ramos cells were infected with ZEBRA-expression lentivirus and positively infected cells were sorted, which were named Ramos-Lv-ZEBRA.
Project description:EBV immediate early protein ZEBRA was corroborated to interact with Pax5 which controls the fate of B cells. Ramos cells were infected with ZEBRA-expression lentivirus and positively infected cells were sorted, which were named Ramos-Lv-ZEBRA.
Project description:Expression data from different expressed genes (DEGs) in human esophageal squamous cell carcinoma (ESCC) EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C) Lysine demethylase 5C (KDM5C), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. KDM5C was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of KDM5C in ESCC cell line.
Project description:To get insight into the mechanisms of MCL1-induced survival and transformation, we screened 41,000 human genes in a genome-wide gene expression profile analysis of MCL1 over-expressing B-NHL cells. Experiment Overall Design: Two-color (Cy5-CTP/ Cy3-CTP) microarray-based gene expression formats presenting high-density oligonucleotide probes printed on a single glass slide were used (Agilent technologies, Cat No# G4112A whole human genome 41K). Total RNAs from MCL1 over-expressing RAMOS RA-1 and Z-138 B-cells were labeled with Cy5-CTP, whereas RNAs from references (empty vector/ RAMOS RA-1 and empty vector/ Z-138 B-cells) were labeled with Cy3-CTP. After competitive hybridization [RNA-Cy5 from MCL1 over-expressing RAMOS RA-1 or MCL1 over-expressing Z-138 versus RNA-Cy3 from either empty vector/ RAMOS RA-1 or empty vector/ Z-138 respectively] gene expression data were pre-processed using Feature Extraction software and GEPAS tools (http://gepas.bioinfo.cipf.es/).
Project description:To further explore the underlying molecular pathways altered by MAP3K3I441M in endothelial cells, the mouse endothelial cell line bEnd.3 was first infected with lentivirus-MAP3K3I441M (LV- MAP3K3I441M-P2A-EGFP; LV-EGFP was used as the control). Total RNA from these cells was then subjected to RNA sequencing.
Project description:In the context of lentiviral vector (LV)-mediated gene correction of hematopoietic stem and progenitor cells (HSPC), the viral origin of LV could trigger cellular responses with potential functional consequences that have not been investigated to date. Here, a time-course genome-wide transcriptional profiling of transduced human HSPC reveals a remarkably limited impact of LV on cellular gene expression, supporting some stealth features of the vector. In particular, LV efficiently escaped innate immune sensing that instead led to robust type I IFN signaling upon transduction with a gamma-retroviral vector. However, recognition of LV DNA prior to integration did trigger DNA damage responses that were activated also by non-integrating Adeno-associated vector DNA. As a consequence of this transient p53 activation, transduced HSPC showed increased apoptosis in vitro and reduced engraftment in vivo at limiting cell doses, but no long-term impact or competitive disadvantage were detected. Pharmacological inhibition of the LV signaling partially rescued both apoptosis and engraftment, potentially providing a novel strategy to further dampen the impact of ex vivo gene therapy on HSPC. Overall, our results shed light on the molecular mechanisms of viral vector sensing in HSPC and provide critical insight for the development of more stealth gene therapy strategies.
Project description:To further development of the effects of miR-200a in ovarian cancer OVCAR3 cells，we have employed lncRNA and mRNA microarray as a discovery platform to identify lncRNA and mRNA expression in miR-200a overexpressing ovarian cancer cells. OVCAR3 cells were transfected with lentiviral vector with eGFP, encoding miR-200a and negative control vector (LV- miR-200a and LV-CON,) by using polybrene. The dysregulation of miR-200a was confirmed by using RT-PCR. RNA was extracted and detected by a lncRNA and mRNA microarray in LV-miR-200a and LV-CON OVCAR3 cells. The different expression of lncRNA and mRNA in LV-miR-200a and LV-CON OVCAR3 cells was analyzed to explore the mechanism that miR-200a affect ovarain cancer cells.
