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Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

ABSTRACT: Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

PROVIDER: PRJNA637227 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11922875.fastq.gz	Fastqsanger.gz
	SRR11922876.fastq.gz	Fastqsanger.gz
	SRR11922877.fastq.gz	Fastqsanger.gz
	SRR11922878.fastq.gz	Fastqsanger.gz
	SRR11922879.fastq.gz	Fastqsanger.gz

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Genome-wide BRD4 occupancy upon expression of YFV capsid in Huh-7 cells

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YFV Capsid changes to mRNA transcriptome of Huh7 cells

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The yellow fever virus capsid protein is a potent suppressor of RNA silencing that binds double stranded RNA.

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RNAseq analysis of BDAA treatment on YFV infected HEK293 cells

Project description:Purpose: to investigate the change in gene expression after BDAA treatment on YFV infected HEK293 cells. Methods: HEK293 cells were cultured; then cells were non-infected/infected with YFV, and then untreat/treat with BDAA. Total RNA were harvested and sent to RNA sequencing. Results: we demonstrated that BDAA treatment of YFV infected HEK293 cells at 18 hpi for 2 h increased expression of a total of 39 cellular genes, 33 of which are inflammatory cytokines, chemokines or ISGs, and the remaining are mostly genes related to NFκB, TNF-α and MAPK signal transduction. Conclusion: BDAA triggers an enhanced activation of RNA sensor-mediated inflammatory cytokine responses, most likely by YFV RNA.

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Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through integrated proteomics and validating studies, we discovered that ZRF1 and BRD4 form a complex with p113, a novel protein derived from CUX1 circular RNA. To investigate the mechanisms underlying the oncogenic functions of ZRF1 and BRD4, we employed the Illumina Novaseq 6000 as a discovery platform to analyze the genome-wide occupancy of ZRF1 and BRD4 on target genes in human SH-SY5Y cells, while the results were further analyzed with p113-regulated target genes. The results showed that 46 target genes were regulated by transcriptional trimer complex p113/ZRF1/BRD4, especially those involved in metabolic pathway or complex I biogenesis, including ALDH3A1, NDUFA1, and NDUFAF5. Furthermore, we validated the ChIP-seq results by real-time PCR with high identity. Overall, our results provided fundamental information about the genomic enrichment of ZRF1 and BRD4 in human NB cells, and these findings will help us understand the pathogenesis of NB.

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