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RNA-seq of hematopoietic stem and progenitor cells from 40 hours post fertilization ddx41 mutant and sibling zebrafish

ABSTRACT: RNA-seq of hematopoietic stem and progenitor cells from 40 hours post fertilization ddx41 mutant and sibling zebrafish

PROVIDER: PRJNA612697 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11309037_1.fastq.gz	Fastqsanger.gz
	SRR11309037_2.fastq.gz	Fastqsanger.gz
	SRR11309038_1.fastq.gz	Fastqsanger.gz
	SRR11309038_2.fastq.gz	Fastqsanger.gz
	SRR11309039_1.fastq.gz	Fastqsanger.gz

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RNA-seq of erythroid cells from 40 hours post fertilization ddx41 mutant and sibling zebrafish

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Project description:Most cases of adult myeloid neoplasms are routinely assumed to be sporadic. Here, we describe an adult familial acute myeloid leukemia (AML) syndrome caused by germline mutations in the DEAD/H-Box helicase gene DDX41. DDX41 was also found to be affected by somatic mutations in sporadic cases of myeloid neoplasms as well as in a biallelic fashion in 50% of patients with germline DDX41 mutations. Moreover, corresponding deletions on 5q35.3 present in 6% of cases lead to haploinsufficient DDX41 expression. DDX41 lesions caused altered pre-mRNA splicing and RNA processing. DDX41 is exemplary of other RNA helicase genes also affected by somatic mutations, suggesting that they constitute a family of tumor suppressor genes. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved diagnostic bone marrow or peripheral blood samples.

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RNA-seq of endothelial cells from 28 hours post fertilization sf3b1 mutant and sibling zebrafish with Stat3 overexpression

Project description:RNA-seq of endothelial cells from 28 hours post fertilization sf3b1 mutant and sibling zebrafish with Stat3 overexpression

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Inherited and somatic defects in DDX41 in myeloid neoplasms

2015-04-01 | GSE66668 | GEO

R-loop proximity proteomics identifies a role of DDX41 in transcription-associated genomic instabilityR-loop proximity proteomics identifies a role of DDX41 in transcription-associated genomic instability

Project description:Transcription can pose a threat to genomic stability through the formation of R-loops that obstruct the progression of replication forks. R-loops are three-stranded nucleic acid structures formed by an RNA-DNA hybrid with a displaced non-template DNA strand. We developed RDProx to identify proteins that regulate R-loops in human cells. RDProx relies on the expression of the hybrid-binding domain (HBD) of Ribonuclease H1 (RNaseH1) fused to the ascorbate peroxidase (APEX2), which permits mapping of the R-loop proximal proteome using quantitative mass spectrometry. We associated R-loop regulation with different cellular proteins and identified a role of the tumor suppressor DEAD box protein 41 (DDX41) in opposing R-loop-dependent genomic instability. Depletion of DDX41 resulted in replication stress, double strand breaks and increased inflammatory signaling. Furthermore, DDX41 opposes accumulation of R-loops at gene promoters and its loss leads to upregulated expression of TGFβ and NOTCH signaling genes. Germline loss-of-function mutations in DDX41 lead to predisposition to acute myeloid leukemia (AML) in adulthood. We propose that accumulation of co-transcriptional R-loops, associated gene expression changes and inflammatory response contribute to the development of familial AML with mutated DDX41.

2021-11-25 | PXD024517 | Pride

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