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DDX17 is involved in DNA damage repair and modifies FUS toxicity in an RGG-domain dependent manner

ABSTRACT: DDX17 is involved in DNA damage repair and modifies FUS toxicity in an RGG-domain dependent manner

PROVIDER: PRJNA727319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14420100.fastq.gz	Fastqsanger.gz
	SRR14420101.fastq.gz	Fastqsanger.gz
	SRR14420102.fastq.gz	Fastqsanger.gz
	SRR14420103.fastq.gz	Fastqsanger.gz
	SRR14420104.fastq.gz	Fastqsanger.gz

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Similar Datasets

DDX17 is involved in DNA damage repair and modifies FUS toxicity in an RGG-domain dependent manner

2021-05-05 | GSE173838 | GEO

DDX17 is involved in DNA damage repair and modifies FUS toxicity in an RGG-domain dependent manner.

Project description:Mutations in the RNA binding protein, Fused in Sarcoma (FUS), lead to amyotrophic lateral sclerosis (ALS), the most frequent form of motor neuron disease. Cytoplasmic aggregation and defective DNA repair machinery are etiologically linked to mutant FUS-associated ALS. Although FUS is involved in numerous aspects of RNA processing, little is understood about the pathophysiological mechanisms of mutant FUS. Here, we employed RNA-sequencing technology in Drosophila brains expressing FUS to identify significantly altered genes and pathways involved in FUS-mediated neurodegeneration. We observed the expression levels of DEAD-Box Helicase 17 (DDX17) to be significantly downregulated in response to mutant FUS in Drosophila and human cell lines. Mutant FUS recruits nuclear DDX17 into cytoplasmic stress granules and physically interacts with DDX17 through the RGG1 domain of FUS. Ectopic expression of DDX17 reduces cytoplasmic mislocalization and sequestration of mutant FUS into cytoplasmic stress granules. We identified DDX17 as a novel regulator of the DNA damage response pathway whose upregulation repairs defective DNA damage repair machinery caused by mutant neuronal FUS ALS. In addition, we show DDX17 is a novel modifier of FUS-mediated neurodegeneration in vivo. Our findings indicate DDX17 is downregulated in response to mutant FUS, and restoration of DDX17 levels suppresses FUS-mediated neuropathogenesis and toxicity in vivo.

| S-EPMC8856901 | biostudies-literature

Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain

Project description:Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain was analyzed during post-exponential phase of growth Keywords: rgg mutant Microarray analysis was performed using RNA samples isolated from both wild-type SF370 and SF370 rgg mutant strains during post-exponential phase of growth

2010-05-26 | E-GEOD-7335 | biostudies-arrayexpress

Rgg-dependent transcriptional regulation in Streptococcus pyogenes strains MGAS5005 and CS101

Project description:Rgg-dependent transcriptional regulation in Streptococcus pyogenes strains MGAS5005 and CS101 was analyzed during post-exponential phase of growth Keywords: strain comparion, post-exponential growth, rgg mutant Microarray analysis was performed using RNA samples isolated from wild-type MGAS5005 and CS101 strains as well as their rgg mutant strains during post-exponential phase of growth

2010-05-26 | E-GEOD-7341 | biostudies-arrayexpress

Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain

Project description:Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain was analyzed during post-exponential phase of growth Keywords: rgg mutant

2008-02-01 | GSE7335 | GEO

Microarray analysis of Rgg-dependent transcriptional regulation in Streptococcus suis serotype 2 strain 05ZYH33

Project description:Streptococcus suis 2 Rgg-dependent transcription was analyzed. Microarray analysis was performed using RNA samples isolated from Streptococcus suis 2 wild-type strain 05ZYH33 as well as RNA isolated from 05ZYH33 rgg isogenic mutant strain during postexponential phases of growth.

2010-06-20 | E-GEOD-21940 | biostudies-arrayexpress

Rgg-dependent transcriptional regulation in Streptococcus pyogenes strains MGAS5005 and CS101

2008-02-01 | GSE7341 | GEO

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

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

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