Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [Pol2_ChIP]

ABSTRACT: Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with P300/CBP and RB proteins. To understand why, experiments with structure-based e1a mutants were analyzed with RNA- and ChIP-seq. The results indicate that e1a displaces RBs from E2F activation domains and, by promoting P300 acetylation of RB1 K873/K874, locks them into a repressing conformation that interacts with repressive chromatin modifying enzymes. e1a then delivers these repressing p300-e1a-RB1 complexes to cell genes that have unusually high P300 association with the gene body, enriched in genes of the TGFb-, TNF-, and IL1-signaling pathways. The P300-e1a-RB complex condenses chromatin, dependent on HDAC activity, P300 lysine acetylase activity, the P300 bromodomain, and acetylation of RB K873/K874 and e1a K239, contributing to repression of host genes that would otherwise inhibit cell cycling. The data suggest why e1a must bind P300/CBP as well as RBs for oncogenic transformation and why a trimeric P300-e1a-RB1 complex is required. Examination of POL II rearrangements by adenoviral e1a in IMR90

ORGANISM(S): Homo sapiens

SUBMITTER: Arnold Berk

PROVIDER: E-GEOD-59691 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [RB1_ChIP]

Project description:Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with P300/CBP and RB proteins. To understand why, experiments with structure-based e1a mutants were analyzed with RNA- and ChIP-seq. The results indicate that e1a displaces RBs from E2F activation domains and, by promoting P300 acetylation of RB1 K873/K874, locks them into a repressing conformation that interacts with repressive chromatin modifying enzymes. e1a then delivers these repressing p300-e1a-RB1 complexes to cell genes that have unusually high P300 association with the gene body, enriched in genes of the TGFb-, TNF-, and IL1-signaling pathways. The P300-e1a-RB complex condenses chromatin, dependent on HDAC activity, P300 lysine acetylase activity, the P300 bromodomain, and acetylation of RB K873/K874 and e1a K239, contributing to repression of host genes that would otherwise inhibit cell cycling. The data suggest why e1a must bind P300/CBP as well as RBs for oncogenic transformation and why a trimeric P300-e1a-RB1 complex is required. Examination of RB1 rearrangements by adenoviral e1a in IMR90

2014-08-15 | E-GEOD-59689 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [RB1_ChIP_2]

2014-08-15 | E-GEOD-59690 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [p300_ChIP]

2014-08-15 | E-GEOD-59681 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [H3k27ac_ChIP]

2014-08-15 | E-GEOD-59680 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [IMR90_Input]

Project description:Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with P300/CBP and RB proteins. To understand why, experiments with structure-based e1a mutants were analyzed with RNA- and ChIP-seq. The results indicate that e1a displaces RBs from E2F activation domains and, by promoting P300 acetylation of RB1 K873/K874, locks them into a repressing conformation that interacts with repressive chromatin modifying enzymes. e1a then delivers these repressing p300-e1a-RB1 complexes to cell genes that have unusually high P300 association with the gene body, enriched in genes of the TGFb-, TNF-, and IL1-signaling pathways. The P300-e1a-RB complex condenses chromatin, dependent on HDAC activity, P300 lysine acetylase activity, the P300 bromodomain, and acetylation of RB K873/K874 and e1a K239, contributing to repression of host genes that would otherwise inhibit cell cycling. The data suggest why e1a must bind P300/CBP as well as RBs for oncogenic transformation and why a trimeric P300-e1a-RB1 complex is required. Chromatin IP background Input DNA for ChIP-seq normalization

2014-08-15 | E-GEOD-59692 | biostudies-arrayexpress

Reorganization of the host epigenome by a viral oncogene

Project description:Adenovirus small e1a causes ~70% reduction in cellular levels of histone H3 lysine 18 acetylation (H3K18ac). It is unclear, however, where this dramatic reduction occurs genome-wide. ChIP-seq revealed that e1a erases 95% of H3K18ac peaks in normal fibroblasts and replaces them with one-third as many at new genomic locations. H3K18ac at promoters and intergenic regions of genes with fibroblast-related functions are relocalized after infection to promoters of highly-induced genes that regulate cell cycling and to new putative enhancers. Strikingly, a significant fraction of the post-infection H3K18ac peaks occurs precisely at regions bound by RB1 in uninfected cells, but not by p107 or p130 without RB1. In contrast, over half of H3K9ac peaks are similarly distributed before and after infection, independently of RB1. The strategic redistribution of H3K18ac by e1a highlights the importance of this modification for transcriptional activation and cellular transformation. Examination of two histone acetylations and RB family members binding. mRNA-Seq RPKM file linked as supplementary file on Series record.

2012-04-04 | E-GEOD-32340 | biostudies-arrayexpress

CBP/P300 Function in Repression as well as Activation Regulated by Adenovirus Small E1A [RNA-seq]

2014-08-15 | E-GEOD-59688 | biostudies-arrayexpress

Adenovirus Small E1A Employs the Lysine Acetylases p300/CBP and Tumor Suppressor Rb to Repress Select Host Genes and Promote Productive Virus Infection [IMR90_Input]

Project description:Oncogenic transformation by adenovirus small e1a depends on simultaneous interactions with the host lysine acetylases p300/CBP and the tumor suppressor RB. How these interactions influence cellular gene expression remains unclear. We find that e1a displaces RBs from E2F transcription factors and promotes p300 acetylation of RB1 K873/K874 to lock it into a repressing conformation that interacts with repressive chromatin-modifying enzymes. These repressing p300-e1a-RB1 complexes specifically interact with host genes that have unusually high p300 association within the gene body. The TGF?-, TNF-, and interleukin-signaling pathway components are enriched among such p300-targeted genes. The p300-e1a-RB1 complex condenses chromatin in a manner dependent on HDAC activity, p300 lysine acetylase activity, the p300 bromodomain, and RB K873/K874 and e1a K239 acetylation to repress host genes that would otherwise inhibit productive virus infection. Thus, adenovirus employs e1a to repress host genes that interfere with viral replication.

2014-08-15 | GSE59692 | GEO

Adenovirus Small E1A Employs the Lysine Acetylases p300/CBP and Tumor Suppressor Rb to Repress Select Host Genes and Promote Productive Virus Infection [Pol2_ChIP]

2014-08-15 | GSE59691 | GEO

Adenovirus Small E1A Employs the Lysine Acetylases p300/CBP and Tumor Suppressor Rb to Repress Select Host Genes and Promote Productive Virus Infection [RB1_ChIP_2]

2014-08-15 | GSE59690 | GEO