E2F1-regulated genes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE498 | GEO | 2003/07/16
SECONDARY ACCESSION(S): PRJNA85203
REPOSITORIES: GEO
Similar Datasets
Project description:Identification of E2F1-regulated genes that modulate the transition from quiescence into DNA synthesis, or have roles in apoptosis, signal transduction, membrane biology, and transcription repression.
2008-06-13 | E-GEOD-498 | biostudies-arrayexpress
Project description:Many cells in our body reside in a reversible nondividing state termed G0 or quiescence. Precise regulation of entry and exit from G0 is critical for maintaining tissue homeostasis. G0 entry can occur when cells do not receive the required signals for cell cycle progression, leading to active repression of cell cycle genes through several mechanisms, including formation of repressor complexes to restrict chromatin accessibility for transcriptional activators. G0 cells can re-enter the G1 phase of the cell cycle upon receiving growth factor signals, resulting in activation of the Mitogen-Activated Protein Kinase pathway, converging on E2F transcription factors. Ectopic expression of E2F1 alone, a transcriptional activator, is sufficient to promote G0 exit without requiring the upstream signals, but it is unclear how E2F1 can overcome the chromatin lockdown in G0 cells to activate cell cycle genes. To better understand this mechanism, we compared dynamics, gene regulation and chromatin accessibility state between E2F1-mediated and growth factor (serum)-induced cell cycle reentry. Using live cell single cell tracking, we observe that E2F1 induction leads to accelerated cell cycle progression compared to regular serum-induced cell cycle re-entry. This accelerated cell cycle re-entry by E2F1 is accompanied by faster upregulation of cell cycle genes. Interestingly, we find that E2F1 preferentially binds to gene promoters that remain in a poised chromatin state after G0 induction, suggesting that G0 cells are prepared for cell cycle re-entry via regulating chromatin states in essential cell cycle genes.
2025-09-26 | GSE296086 | GEO
Project description:Many cells in our body reside in a reversible nondividing state termed G0 or quiescence. Precise regulation of entry and exit from G0 is critical for maintaining tissue homeostasis. G0 entry can occur when cells do not receive the required signals for cell cycle progression, leading to active repression of cell cycle genes through several mechanisms, including formation of repressor complexes to restrict chromatin accessibility for transcriptional activators. G0 cells can re-enter the G1 phase of the cell cycle upon receiving growth factor signals, resulting in activation of the Mitogen-Activated Protein Kinase pathway, converging on E2F transcription factors. Ectopic expression of E2F1 alone, a transcriptional activator, is sufficient to promote G0 exit without requiring the upstream signals, but it is unclear how E2F1 can overcome the chromatin lockdown in G0 cells to activate cell cycle genes. To better understand this mechanism, we compared dynamics, gene regulation and chromatin accessibility state between E2F1-mediated and growth factor (serum)-induced cell cycle reentry. Using live cell single cell tracking, we observe that E2F1 induction leads to accelerated cell cycle progression compared to regular serum-induced cell cycle re-entry. This accelerated cell cycle re-entry by E2F1 is accompanied by faster upregulation of cell cycle genes. Interestingly, we find that E2F1 preferentially binds to gene promoters that remain in a poised chromatin state after G0 induction, suggesting that G0 cells are prepared for cell cycle re-entry via regulating chromatin states in essential cell cycle genes.
2025-09-26 | GSE296085 | GEO
Project description:Many cells in our body reside in a reversible nondividing state termed G0 or quiescence. Precise regulation of entry and exit from G0 is critical for maintaining tissue homeostasis. G0 entry can occur when cells do not receive the required signals for cell cycle progression, leading to active repression of cell cycle genes through several mechanisms, including formation of repressor complexes to restrict chromatin accessibility for transcriptional activators. G0 cells can re-enter the G1 phase of the cell cycle upon receiving growth factor signals, resulting in activation of the Mitogen-Activated Protein Kinase pathway, converging on E2F transcription factors. Ectopic expression of E2F1 alone, a transcriptional activator, is sufficient to promote G0 exit without requiring the upstream signals, but it is unclear how E2F1 can overcome the chromatin lockdown in G0 cells to activate cell cycle genes. To better understand this mechanism, we compared dynamics, gene regulation and chromatin accessibility state between E2F1-mediated and growth factor (serum)-induced cell cycle reentry. Using live cell single cell tracking, we observe that E2F1 induction leads to accelerated cell cycle progression compared to regular serum-induced cell cycle re-entry. This accelerated cell cycle re-entry by E2F1 is accompanied by faster upregulation of cell cycle genes. Interestingly, we find that E2F1 preferentially binds to gene promoters that remain in a poised chromatin state after G0 induction, suggesting that G0 cells are prepared for cell cycle re-entry via regulating chromatin states in essential cell cycle genes.
2025-09-26 | GSE296087 | GEO
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.
2015-12-01 | GSE74006 | GEO
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.
2025-06-12 | GSE284473 | GEO
Project description:The long non-coding RNA SLNCR and the transcription factor E2F1 both have oncogenic activities in melanoma. Here we show that melanoma metastasis depends upon the formation of an oncogenic SLNCR–E2F1 complex. Unbiased computational analyses of patient samples revealed worse overall survival only in melanoma patients overexpressing both SLNCR and E2F1. Blocking SLNCR–E2F1 complex formation without reducing the levels of either SLNCR or E2F1 reversed melanoma invasion ex vivo and melanoma extravasation in mice. We discovered that E2F1 bound to sequences in SLNCR that are the RNA analogs of the E2F consensus DNA-binding element, suggesting that RNA and DNA binding engages the same domain in E2F1. Binding competition assays demonstrated that E2F1 preferentially bound to RNA compared to its cognate DNA element and that RNA efficiently competed with the consensus DNA-binding element for E2F1 binding. Molecular dynamics simulations indicated increased thermodynamic stability of E2F1–DNA interactions as compared to E2F1–RNA interactions. However, molecular dynamics simulations also indicated greater number of RNA-amino acid contacts within the E2F1 DNA binding domain (E2F1DBD) than DNA. This suggests better kinetic binding properties of RNA to the E2F1DBD as compared to DNA and may explain how RNA efficiently competed with DNA for E2F1DBD binding. E2F1 often binds to DNA as a heterodimer with DP1. Molecular dynamics simulations suggested that RNA binding to E2F1 may prevent E2F1–DP1 heterodimerization by masking key amino acids required for DP1 binding. These data reveal the SLNCR-driven oncogenic activities of E2F1 and identify the SLNCR–E2F1 complex as a target for future melanoma therapy.
2025-06-17 | GSE270372 | GEO
Project description:1. To identify potential effectors responsible for anti-tumorigenesis by targeting PLD1, we performed microarray in two Wnt-relevant colon cancer cells and analyzed transcriptional profile of genes that were differently expressed by inhibition and knockdown of PLD1 2. We also investigated potential downstream effectors of PLD1-E2F1 axis using microarray analysis in PLD1 and E2F1-depleted CRC cells.
2015-06-03 | GSE55724 | GEO
Project description:Effect of FOXO knockdown on E2F1-mediated transcription
2012-07-06 | GSE39136 | GEO
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