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Homo sapiens

ABSTRACT: MYCL and EP400 are required for Max and MCPyV mediated gene activation

PROVIDER: PRJNA390939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5712080.fastq.gz	Fastqsanger.gz
	SRR5712090.fastq.gz	Fastqsanger.gz
	SRR5712081.fastq.gz	Fastqsanger.gz
	SRR5712091.fastq.gz	Fastqsanger.gz
	SRR5712082.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:EP400 is required for Max and MCPyV mediated gene activation

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MCPyV ST, MAX and the TRRAP complex cooperate to bind to Transcription Start Sites

Project description:To determine if MCPyV ST was recruited to chromatin together with MAX and the TRRAP complex, we performed chromatin immunoprecipitation (ChIP) using the validated antibodies to MCPyV ST produced in our lab, HA tagged ST, MAX and EP400 followed by next generation sequencing. De novo DNA motif analysis revealed that the canonical E-box MYC target sequence was the most frequently observed motif. Metagene analysis revealed that antibodies to MAX, EP400, ST (Ab5) and HA tagged ST showed strong enrichment in transcription start site (TSS). H3K4me3 ChIP-seq confirmed that the peaks enriched with antibodies to MAX, EP400 and ST all centered on the H3K4me3 peaks with a high degree of overlap.

2017-09-28 | GSE69877 | GEO

MYCL and EP400 are required for Max and MCPyV mediated gene activation

Project description:To determine if MYCL or EP400 knockdown would affect Max target genes in Merkel cell carcinoma cell line MKL-1, we performed RNA-seq analyses of MKL-1 cells inducibly expressing shMYCL and two different EP400 shRNA -2, -3 and compared to ChIP-seq data using BETA analyses.

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Merkel cell polyomavirus small T antigen promotes pro-glycolytic metabolic perturbations required for transformation

Project description:Merkel cell polyomavirus (MCPyV) is an etiological agent of Merkel cell carcinoma (MCC), a highly aggressive skin cancer. The MCPyV small tumor antigen (ST) is required for maintenance of MCC and can transform normal cells. To gain insight into cellular perturbations induced by MCPyV ST, we performed transcriptome analysis of normal human fibroblasts with inducible expression of ST. MCPyV ST dynamically alters the cellular transcriptome with increased levels of glycolytic genes, including the monocarboxylate lactate transporter SLC16A1 (MCT1). Extracellular flux analysis revealed increased lactate export reflecting elevated aerobic glycolysis in ST expressing cells. Inhibition of MCT1 activity suppressed the growth of MCC cell lines and impaired MCPyV-dependent transformation of IMR90 cells. Both NF-κB and MYC have been shown to regulate MCT1 expression. While MYC was required for MCT1 induction, MCPyV-induced MCT1 levels decreased following knockdown of the NF-κB subunit RelA, supporting a synergistic activity between MCPyV and MYC in regulating MCT1 levels. Several MCC lines had high levels of MYCL and MYCN but not MYC. Increased levels of MYCL was more effective than MYC or MYCN in increasing extracellular acidification in MCC cells. Our results demonstrate the effects of MCPyV ST on the cellular transcriptome and reveal that transformation is dependent, at least in part, on elevated aerobic glycolysis.

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MCPyV ST activates Max target genes by recruiting TRRAP/EP400 complex

Project description:MCPyV ST activates Max target genes by recruiting TRRAP/EP400 complex

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Project description:EP400 Deposits H3.3 into Promoters and Enhancers During Gene Activation

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EP400 is required for Max and MCPyV mediated gene activation

Project description:To determine if EP400 knockdown would affect Max target genes in Merkel cell carcinoma cell line MKL-1, we performed RNA-seq analyses of MKL-1 cells inducibly expressing EP400 shRNA and compared to ChIP-seq data using BETA analyses.

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