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DRIP-seq files for: DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci

ABSTRACT: DRIP-seq files for: DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci

PROVIDER: PRJEB46687 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6384620_1.fastq.gz	Fastqsanger.gz
	ERR6384620_2.fastq.gz	Fastqsanger.gz
	ERR6384621_1.fastq.gz	Fastqsanger.gz
	ERR6384621_2.fastq.gz	Fastqsanger.gz
	ERR6384622_1.fastq.gz	Fastqsanger.gz

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DRIP-seq files for: DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci

Project description:Determining the role of DDX17 in the formation of DNA:RNA-hybrids around active DNA double-strand breaks (DSBs) using DRIP-seq in the damaged induced via AsiSI (DIvA) cell system that induced DSBs at known genomic loci in response to hydroxytamoxifen (OHT) treatment via and AsiSI enzyme fused to an oestrogen receptor. Sequencing was done using either control or DDX17 siRNA, and mock or 4 hours 300nM OHT treatment. Paired-end 150 cycles was completed on an Illumina NextSeq 500 and library prep was completed using the NEB NEBNext Ultra II library prep kit.

2022-11-08 | E-MTAB-10814 | biostudies-arrayexpress

DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.

Project description:Proteins with RNA-binding activity are increasingly being implicated in DNA damage responses (DDR). Additionally, DNA:RNA-hybrids are rapidly generated around DNA double-strand breaks (DSBs), and are essential for effective repair. Here, using a meta-analysis of proteomic data, we identify novel DNA repair proteins and characterise a novel role for DDX17 in DNA repair. We found DDX17 to be required for both cell survival and DNA repair in response to numerous agents that induce DSBs. Analysis of DSB repair factor recruitment to damage sites suggested a role for DDX17 early in the DSB ubiquitin cascade. Genome-wide mapping of R-loops revealed that while DDX17 promotes the formation of DNA:RNA-hybrids around DSB sites, this role is specific to loci that have low levels of pre-existing hybrids. We propose that DDX17 facilitates DSB repair at loci that are inefficient at forming DNA:RNA-hybrids by catalysing the formation of DSB-induced hybrids, thereby allowing propagation of the damage response.

| S-EPMC9561282 | biostudies-literature

DRIP-sequencing U2OS

Project description:DRIP-sequencing U2OS

| PRJNA533125 | ENA

DEAD-box helicase 17 (DDX17) protects cardiac function by promoting mitochondrial homeostasis in heart failure

Project description:DEAD box 17 (DDX17) is a typical member of the DEAD box family with transcriptional cofactor activity. Although DDX17 is abundantly expressed in the myocardium, its role in the heart is not fully understood. We generated cardiomyocyte-specific Ddx17-knockout mice and cardiomyocyte-specific Ddx17 transgenic mice and explored the function of DDX17 using various cardiomyocyte injury and heart failure (HF) models. We also validated the correlation between DDX17 expression and cardiac function in myocardial biopsy samples from HF patients. DDX17 was downregulated in myocardial samples from HF mouse models and cardiomyocyte injury models. We found that the cardiomyocyte-specific knockout of DDX17 promotes autophagic flux blockage and cardiomyocyte apoptosis in pathological conditions, resulting in progressive heart dysfunction, thereby leading to maladaptive remodeling and progression of HF. The replenishment of DDX17 in cardiomyocytes protected heart function in pathological conditions. Further studies showed that DDX17 can bind to the transcriptional repressor BCL6 and inhibit the expression of the mitochondrial fission protein DRP1. When DDX17 expression was decreased, the transcriptional repression of BCL6 was reduced, resulting in increased DRP1 expression and mitochondrial fission, which caused autophagy flux blockage and apoptosis in cardiomyocytes, leading to impaired mitochondrial homeostasis and HF. We also verified the clinical correlation of DDX17 expression with cardiac function and DRP1 expression in endomyocardial biopsies from patients with HF. These findings suggest that DDX17 protects cardiac function by promoting mitochondrial homeostasis through the BCL6-DRP1 pathway during HF.

2024-04-07 | GSE157135 | GEO

LCLF1.0 fastq-Files

Project description:LCLF1.0 fastq-Files

| PRJNA928832 | ENA

LCLF1.0 fastq-Files

Project description:LCLF1.0 fastq-Files

| PRJNA928833 | ENA

Hungarian BAM files

Project description:Hungarian BAM files

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Transcriptome analysis of neuroblastoma SH-SY5Y cells upon DDX17 helicase knock-down

Project description:DDX17 is a DEAD-box RNA helicase protein which is involved in many aspects of RNA metabolism, from gene transcription to RNA processing and decay. As a simple approach to identify DDX17 target genes, we carried out a transcriptome analysis of the human neuroblastoma cell line SH-SY5Y following DDX17 gene knock-down

2024-09-30 | GSE223072 | GEO

downregulation of DDX5 and DDX17

Project description:RNAseq : MCF-7 cells were transfected with siRNA targeting both DDX5 and DDX17 RNA helicases, and total RNA were extracted as described previously (Dardenne Cell Rep 2014).

2017-02-02 | GSE94372 | GEO

SINE RNAs trigger noncanonical NLRC4 inflammasome via DDX17

Project description:Short interspersed element (SINE) RNAs are upregulated by cellular stresses1 (heat shock, DNA damage and viral infection) and accumulate in human diseases (macular degeneration2, lupus3, and Alzheimer’s disease4). These transcripts activate inflammasomes5, a family of cytoplasmic multiprotein complexes that sense danger molecules and initiate innate immune responses by activating caspase-1-dependent cytokine production and inflammatory death6, but the molecular sensor of SINE RNAs is unknown. Here, we identify DDX17, a member of the DEAD box family of RNA helicases7, as a sensor of SINE RNAs requisite for inflammasome activation. Induction of caspase-1 cleavage and release of IL-1 and IL-18 by SINE RNAs requires dual recruitment of NLRP3 and NLRC4 but proceeds independent of NAIPs, immune sensors required for canonical NLRC4 activation by bacterial proteins8,9. Instead, SINE RNAs trigger DDX17–NLRC4 interaction, which licenses inflammasome activation. We also report increased levels of DDX17 protein and association of DDX17 and NLRC4 in the retinal pigmented epithelium (RPE) of human eyes with an advanced, untreatable form of age-related macular degeneration (AMD). Disrupting DDX17–NLRC4 signalling blocks SINE RNA-induced inflammasome activation in human RPE cells and RPE degeneration in an animal model of AMD. Our findings uncover a non-canonical mode of inflammasome activation by endogenous retrotransposon transcripts, and provide new potential targets for macular degeneration and potentially other diseases.

2022-06-09 | PXD016019 | Pride

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