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Next Generation Sequencing Facilitates Quantitative Analysis of ChIP-sequence of U2OS cells expressing FANCD2-3x FLAG under mild replication stress by low dose aphidicolin (APH)

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of ChIP-sequence of U2OS cells expressing FANCD2-3x FLAG under mild replication stress by low dose aphidicolin (APH)

PROVIDER: PRJNA412775 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6122930_1.fastq.gz	Fastqsanger.gz
	SRR6122930_2.fastq.gz	Fastqsanger.gz
	SRR6122931_1.fastq.gz	Fastqsanger.gz
	SRR6122931_2.fastq.gz	Fastqsanger.gz
	SRR6122932_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of ChIP-sequence of U2OS cells expressing FANCD2-3x FLAG under mild replication stress by low dose aphidicolin (APH)

Project description:Genome-wide distribution of FANCD2 protein in chromatin under replication stress.

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of human U2OS cells under mild replication stress by low dose aphidicolin (APH)

Project description:To detect transcripts before and after APH treatment, we subjected total RNA isolated from U2OS cells expressing human FANCD2-3xFLAG to next generation sequencing.

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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of human U2OS cells under mild replication stress by low dose aphidicolin (APH)

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FANCD2 Activates Transcription of TAp63 and Suppresses Tumorigenesis

Project description:Fanconi Anemia (FA) is a rare genetic disorder characterized by an increased susceptibility to squamous cell cancers. Fifteen FA genes are known, and the encoded proteins cooperate in a common DNA repair pathway. A critical step is the monoubiquitination of the FANCD2 protein, and cells from most FA patients are deficient in this step. How monoubiquitinated FANCD2 suppresses squamous cell cancers is unknown. Here we show that Fancd2-deficient mice are prone to Ras oncogene-driven skin carcinogenesis, while Usp1-deficient mice, expressing elevated cellular levels of Fancd2-Ub, are resistant to skin tumors. Moreover, Fancd2-Ub activates the transcription of the tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis. For FA patients, the reduction of FANCD2-Ub and TAp63 protein levels may account for their susceptibility to squamous cell neoplasia. Taken together, Usp1 inhibition may be a useful strategy for upregulating TAp63 and preventing or treating squamous cell cancers in the general non-FA population. Examination of FANCD2 binding after UV treatment in 293T cells

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Project description:Map the origins of DNA replication in human cells at 7 common fragile sites and their flanking non-fragile sequences as well as a 200kb containing the rare fragile site FRAXA, and a 1,075kb non-fragile region on chr22 . The origins were mapped in untreated cells, as well as, in cells treated with aphidicolin (APH), trichostatin A (TSA), or APH plus TSA. The origin mapping experiment is based on the fact that during S phase, short newly replicated DNA fragments (300bp-1kb) are generated only at the origins of replication. By combining the nascent strand assay with a tiled microarray platform, we have previoulsy developed a rapid, non-PCR based, high-throughput approach to map active origins in asynchronous human cells (Lucas et al., 2007, AC 17668008).

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