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ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

ABSTRACT: ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

PROVIDER: PRJNA540499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8992350.fastq.gz	Fastqsanger.gz
	SRR8992351.fastq.gz	Fastqsanger.gz
	SRR8992352.fastq.gz	Fastqsanger.gz
	SRR8992353.fastq.gz	Fastqsanger.gz
	SRR8992354.fastq.gz	Fastqsanger.gz

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ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

Project description:To evaluate the effects of cordycepin on CRY2 and RUVBL2 binding on the chromatin sites, non-synchronized U2OS cells were treated with cordycepin (100 uM) for 1 h, then performed ChIP-seq. We found that cordycepin relieves CRY2 and RUVBL2 proteins from the chromatin for more than 60-70%.

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Project description:Transcription regulators and apparatuses compartmentalize into transcriptional condensates in part through molecular interactions among intrinsically disordered regions. To better understand how these fundamental condensates are regulated, we performed time-series analyses of transcriptome, genome and imaging to show that the previously characterized molecular chaperone RUVBL2 assembles Pol II condensates by its ATPase activity and prevalently interacting with diverse oncogenic transcription factors at promoters, thereby maintaining active transcription in mammalian cells. Besides, RUVBL2 is overexpressed in various cancers, has higher expression levels and preferential chromatin binding compared with RUVBL1. Remarkably, acute protein degradation and chemical perturbations of RUVBL2 with the nucleoside compound cordycepin result in the repression of oncogenes in embryonic stem cells and breast cancer cells, respectively. Our results suggest that molecular chaperone RUVBL2 safeguards the hemostasis of transcriptional condensates at promoters. Thus, pharmacological perturbations of RUVBL2 is a promising strategy to restore these condensates in breast cancers.

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