E2F4 and Myc ChIP-chip perfomed on Nimblegen hg17 ENCODE arrays
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE6375 | GEO | 2007/01/20
REPOSITORIES: GEO
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Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. In order to fully understand the physiological roles of E2F4 and the regulatory networks it mediates, and to reveal its relationships with other members of the E2F family, it is essential to comprehensively identify E2F4 target sites throughout the genome. Here, we investigated genome-wide E2F4 targets in human lymphoblastoid cells using the recently developed unbiased target discovery technique of ChIP sequencing. We sequecned E2F4 ChIP and corresponding Input
2010-11-01 | E-GEOD-21488 | biostudies-arrayexpress
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. In order to fully understand the physiological roles of E2F4 and the regulatory networks it mediates, and to reveal its relationships with other members of the E2F family, it is essential to comprehensively identify E2F4 target sites throughout the genome. Here, we investigated genome-wide E2F4 targets in human lymphoblastoid cells using the recently developed unbiased target discovery technique of ChIP sequencing.
2010-11-01 | GSE21488 | GEO
Project description:Deregulation of RNA polymerase II (RNAPII) by oncoproteins, such as transcription factor Myc, interferes with DNA replication and is a major source of DNA damage and genomic instability. Ubiquitination is a key pathway controlling RNAPII activity via modification of RNAPII subunits or associated regulatory proteins. We uncover a mechanism for genome maintenance by ubiquitin ligase Trim33 and transcription factor E2f4. We show that Trim33 promotes E2f4 protein turnover, restricting interactions of E2f4 with chromatin and with the Recql DNA helicase. Replicative stress blunts Trim33-dependent regulation, which stimulates Recql recruitment to chromatin and facilitates recovery of DNA synthesis. Deletion of Trim33 triggers chronic recruitment of Recql and accelerates DNA replication under stress, accompanied by compromised DDR signaling and DNA repair. Depletion of Trim33 in Myc-overexpressing cells leads to accumulation of replication-associated DNA damage and delays Myc-driven tumorigenesis. We propose that the Trim33-E2f4-Recql axis provides a mechanism to control DNA replication at transcriptionally active chromatin to maintain genome integrity.
2023-07-28 | GSE217521 | GEO
Project description:Deregulation of RNA polymerase II (RNAPII) by oncoproteins, such as transcription factor Myc, interferes with DNA replication and is a major source of DNA damage and genomic instability. Ubiquitination is a key pathway controlling RNAPII activity via modification of RNAPII subunits or associated regulatory proteins. We uncover a mechanism for genome maintenance by ubiquitin ligase Trim33 and transcription factor E2f4. We show that Trim33 promotes E2f4 protein turnover, restricting interactions of E2f4 with chromatin and with the Recql DNA helicase. Replicative stress blunts Trim33-dependent regulation, which stimulates Recql recruitment to chromatin and facilitates recovery of DNA synthesis. Deletion of Trim33 triggers chronic recruitment of Recql and accelerates DNA replication under stress, accompanied by compromised DDR signaling and DNA repair. Depletion of Trim33 in Myc-overexpressing cells leads to accumulation of replication-associated DNA damage and delays Myc-driven tumorigenesis. We propose that the Trim33-E2f4-Recql axis provides a mechanism to control DNA replication at transcriptionally active chromatin to maintain genome integrity.
2023-07-28 | GSE217519 | GEO
Project description:Deregulation of RNA polymerase II (RNAPII) by oncoproteins, such as transcription factor Myc, interferes with DNA replication and is a major source of DNA damage and genomic instability. Ubiquitination is a key pathway controlling RNAPII activity via modification of RNAPII subunits or associated regulatory proteins. We uncover a mechanism for genome maintenance by ubiquitin ligase Trim33 and transcription factor E2f4. We show that Trim33 promotes E2f4 protein turnover, restricting interactions of E2f4 with chromatin and with the Recql DNA helicase. Replicative stress blunts Trim33-dependent regulation, which stimulates Recql recruitment to chromatin and facilitates recovery of DNA synthesis. Deletion of Trim33 triggers chronic recruitment of Recql and accelerates DNA replication under stress, accompanied by compromised DDR signaling and DNA repair. Depletion of Trim33 in Myc-overexpressing cells leads to accumulation of replication-associated DNA damage and delays Myc-driven tumorigenesis. We propose that the Trim33-E2f4-Recql axis provides a mechanism to control DNA replication at transcriptionally active chromatin to maintain genome integrity.
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Project description:Deregulation of RNA polymerase II (RNAPII) by oncoproteins, such as transcription factor Myc, interferes with DNA replication and is a major source of DNA damage and genomic instability. Ubiquitination is a key pathway controlling RNAPII activity via modification of RNAPII subunits or associated regulatory proteins. We uncover a mechanism for genome maintenance by ubiquitin ligase Trim33 and transcription factor E2f4. We show that Trim33 promotes E2f4 protein turnover, restricting interactions of E2f4 with chromatin and with the Recql DNA helicase. Replicative stress blunts Trim33-dependent regulation, which stimulates Recql recruitment to chromatin and facilitates recovery of DNA synthesis. Deletion of Trim33 triggers chronic recruitment of Recql and accelerates DNA replication under stress, accompanied by compromised DDR signaling and DNA repair. Depletion of Trim33 in Myc-overexpressing cells leads to accumulation of replication-associated DNA damage and delays Myc-driven tumorigenesis. We propose that the Trim33-E2f4-Recql axis provides a mechanism to control DNA replication at transcriptionally active chromatin to maintain genome integrity.
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Project description:Deregulation of RNA polymerase II (RNAPII) by oncoproteins, such as transcription factor Myc, interferes with DNA replication and is a major source of DNA damage and genomic instability. Ubiquitination is a key pathway controlling RNAPII activity via modification of RNAPII subunits or associated regulatory proteins. We uncover a mechanism for genome maintenance by ubiquitin ligase Trim33 and transcription factor E2f4. We show that Trim33 promotes E2f4 protein turnover, restricting interactions of E2f4 with chromatin and with the Recql DNA helicase. Replicative stress blunts Trim33-dependent regulation, which stimulates Recql recruitment to chromatin and facilitates recovery of DNA synthesis. Deletion of Trim33 triggers chronic recruitment of Recql and accelerates DNA replication under stress, accompanied by compromised DDR signaling and DNA repair. Depletion of Trim33 in Myc-overexpressing cells leads to accumulation of replication-associated DNA damage and delays Myc-driven tumorigenesis. We propose that the Trim33-E2f4-Recql axis provides a mechanism to control DNA replication at transcriptionally active chromatin to maintain genome integrity.
2023-07-28 | GSE235671 | GEO
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. We investigated the genome-wide binding profile of E2F4 using a newly developed peak calling program based on a kernel density estimation and identified approximately 16 thousands E2F4 binding sites at a 1% FDR threshold, which potentially modulate 7,346 downstream target genes. Gene Ontology (GO) functional analysis of E2F4 target genes revealed several novel functions of E2F4 including I-kappaB kinase/NF-kappaB cascade, protein transport and targeting, protein folding, and sterol biosynthetic process. In addition to mRNA target genes, E2F4 also binds and regulates some miRNA targets such as let-7a, mir-17 and mir-22. Interestingly, we found that about 20% of E2F4 sites are in intergenic regions, which suggests that E2F4 may function at enhancer sites. De novo motif discovery revealed 5 novel, significantly enriched motifs within E2F4 sites. Only 5% of binding sites contain a canonical motif, indicating that E2F4 can use diverse motifs to bind DNA and regulate transcription. Overexpression of E2F4 and its cofactors such as RBL2 and DP-1, followed by microarray analysis, revealed that E2F4 functions as an activator and a repressor. Taken together, our genome-wide E2F4 ChIP sequencing data provided evidences of versatile physiological roles of E2F4 and insights into its functions. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2010-11-01 | E-GEOD-21489 | biostudies-arrayexpress
Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. We investigated the genome-wide binding profile of E2F4 using a newly developed peak calling program based on a kernel density estimation and identified approximately 16 thousands E2F4 binding sites at a 1% FDR threshold, which potentially modulate 7,346 downstream target genes. Gene Ontology (GO) functional analysis of E2F4 target genes revealed several novel functions of E2F4 including I-kappaB kinase/NF-kappaB cascade, protein transport and targeting, protein folding, and sterol biosynthetic process. In addition to mRNA target genes, E2F4 also binds and regulates some miRNA targets such as let-7a, mir-17 and mir-22. Interestingly, we found that about 20% of E2F4 sites are in intergenic regions, which suggests that E2F4 may function at enhancer sites. De novo motif discovery revealed 5 novel, significantly enriched motifs within E2F4 sites. Only 5% of binding sites contain a canonical motif, indicating that E2F4 can use diverse motifs to bind DNA and regulate transcription. Overexpression of E2F4 and its cofactors such as RBL2 and DP-1, followed by microarray analysis, revealed that E2F4 functions as an activator and a repressor. Taken together, our genome-wide E2F4 ChIP sequencing data provided evidences of versatile physiological roles of E2F4 and insights into its functions. This SuperSeries is composed of the SubSeries listed below.
2010-11-01 | GSE21489 | GEO
Project description:E2F transcription factors are central regulators of cell cycle progression and cell fate decisions in mammalian cells. E2F4 is a transcriptional repressor implicated in cell cycle arrest and whose repressive activity depends on its interaction with members of the RB family. E2F4 often represents the predominant E2F activity in cells. Here we show that E2F4 is important for the proliferation and the survival of mouse embryonic stem cells. In these cells, E2F4 acts in part as a transcriptional activator that promotes the expression of cell cycle genes. Importantly, this role for E2F4 is completely independent of the RB family. Accordingly, an unbiased analysis of the E2F4 interactome shows that E2F4 functionally interacts with chromatin regulators associated with gene activation in RB family-mutant cells. Taken together, our findings uncover a non-canonical role for E2F4 that reveal novel insights into the biology of rapidly dividing cell types.
2019-04-26 | PXD008796 | Pride