Project description:Effect of FOXO knockdown on E2F1-mediated transcription U2OS cells stably expressing ER-E2F1 were infected with two different lentiviruses both targeting FOXO1 and FOXO3 or control virus encoding scrambled sequence. Twenty four hours post infection medium was replaced to serum-free DMEM for 24 hours. Then medium was replaced to serum-free DMEM with or without 20 nM 4-hydroxy tamoxifen for 6 hours.
Project description:E2F1 induces numerous genes, including transcription factors, upon activation. The transcription factors then further cooperates with E2F1 to regulate the target genes and enhance the transcriptional effect. We used microarrays to analyze genes upregulated upon E2F1 activation by OHT with and without knockdown of NFYB and identified genes that are targets of both transcription factors.
Project description:Our computational approach identified E2F1 as a potential collaborator of EZH2 in androgen-independent prostate cancer. This experiment is to designed to validate the crosstalking of E2F1 and EZH2 pathways. We showed that majority of the EZH2-induced genes in androgen-independent prostate tumor cells are in downstream of E2F1, providing insight into the EZH2-E2F1 collaborative regulatory pathway.
Project description:E2F1, a member of E2F family transcription factors, is involved in the transcriptional regulation of genes required for G1 to S phase transition of the cell cycle, DNA replication and DNA repair along with apoptosis in response to DNA damage signals. Studies suggest that several DNA viruses deregulate E2F1 functions to modulate their replications. Our previous global transcriptomic analyses (GSE235941, GSE237484) reveal that E2F1 expression is transcriptionally activated during EBV latent infection in naïve B-lymphocytes but suppressed during reactivation into lytic-cycle replication. We hypothesize that EBV controls E2F1 expression to regulate its latent to lytic switch. To gain insights into the E2F1 mediated global transcriptional network of both cell and viral gene expressions in response to EBV lytic cycle induction, we knocked-down E2F1 in EBV positive P3HR1 cells and subjected to RNA-Seq analyses with or without lytic cycle inducer. The primary goals of our work were to identify the key cell pathways and the differential expression patterns of EBV latent and lytic genes upon E2F1 depletion. Our findings support the hypothesis that EBV controls latent to lytic switch by critically monitoring E2F1 expression, providing clues for therapeutic intervention.
Project description:E2F transcription factors are known regulators of the cell cycle, proliferation, apoptosis and differentiation. We reveal an essential role for E2F1 in liver through the regulation of glycolysis and lipogenesis. E2F1 deficiency leads to a decreased in glycolysis and de novo synthesis of fatty acids in hepatocytes. ChIP-Seq was performed to determine direct tagets of E2F1 in hepatocytes. We highlight that E2F1 directly binds the promoters of genes implicated in metabolic process and notably key lipogenic genes to control these pathways.
Project description:We performed RNA-seq for WT and foxo mutant flies, by combining with Dr. Baihua's foxo chip-seq data, we found 101 foxo-repressed and 300 foxo-activated genes. By analyzing expression change of these genes during age, we found foxo-repressed genes became activated, while foxo-activated genes became repressed, suggesting foxo signaling declines with age.
Project description:To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.
Project description:To have a global picture of the miRNAs dependent on the transcription factor E2F1, we assessed small RNA changes, by RNA-sequencing, of HeLa cells transfected with an siRNA targeting E2F1 or a control siRNA.
Project description:In a murine model of high-fat diet, Mx1-Cre was used to induce knockdown of forkhead box O 1,3 and 4 (FoxO 1,3 and 4) in the endothelium of adult mice. Skeletal muscle gene-expression was assessed after 8 weeks of high-fat diet in wild type versus FoxO knockdown mice.