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Danio rerio

ABSTRACT: TP53 modulates oxidative stress in Gata1+ erythroid cells

PROVIDER: PRJNA358512 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5125630_1.fastq.gz	Fastqsanger.gz
	SRR5125630_2.fastq.gz	Fastqsanger.gz
	SRR5125640_1.fastq.gz	Fastqsanger.gz
	SRR5125640_2.fastq.gz	Fastqsanger.gz
	SRR5125621_1.fastq.gz	Fastqsanger.gz

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TP53 modulates oxidative stress in Gata1+ erythroid cells

Project description:In this report, we have found that gata1 expressing erythroid cells contribute to a significant proportion of total body oxidative stress when animals were exposed to a strong pro-oxidant. RNA-seq of zebrafish under oxidative stress revealed the induction of tp53. Zebrafish carrying tp53 with mutation in its DNA binding domain were acutely sensitive to pro-oxidant exposure and displayed significant reactive oxygen species (ROS) and tp53-independent erythroid cell death resulting in an edematous phenotype. We found that a major contributing factor to ROS was increased basal mitochondrial respiratory rate without reserve. These data add to the concept that tp53, while classically a tumor suppressor and cell cycle regulator, has additional roles in controlling cellular oxidative stress.

2017-02-15 | GSE92754 | GEO

GNPS - Lipidomics of GATA1 mutant cells during erythroid maturation

Project description:RP-LC-MS lipidomics data was collected to understand the role of GATA1 during erythroid maturation. GATA1 mutants and WT cells were treated with or without beta-estradiol. GATA1 mutant cells were additionally treated with or without 5-ALA.

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Inactivation of the nuclear interacting SET domain protein 1 (NSD1) impairs GATA1-regulated erythroid differentiation and causes erythroleukemia

Project description:Nuclear receptor binding SET domain protein 1 (NSD1) is recurrently mutated in human cancers including acute leukemia. We found that NSD1 knockdown altered erythroid clonogenic growth of human CD34+ hematopoietic cells. Ablation of Nsd1 in the hematopoietic system induced a transplantable erythroleukemia in mice. Despite abundant expression of the transcriptional master regulator GATA1, in vitro differentiation of Nsd1-/- erythroblasts was majorly impaired associated with reduced activation of GATA1-induced targets, while GATA1-repressed target genes were less affected. Retroviral expression of wildtype Nsd1, but not a catalytically-inactive Nsd1N1918Q SET-domain mutant induced terminal maturation of Nsd1-/- erythroblasts. Despite similar GATA1 levels, exogenous Nsd1 but not Nsd1N1918Q significantly increased GATA1 chromatin occupancy and target gene activation. Notably, Nsd1 expression reduced the association of GATA1 with the co-repressor SKI, and knockdown of SKI induced differentiation of Nsd1-/- erythroblasts. Collectively, we identified the NSD1 methyltransferase as a novel regulator of GATA1-controlled erythroid differentiation and leukemogenesis.

2020-04-08 | PXD017657 | Pride

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [3]

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [4]

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [6]

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [1]

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [5]

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Project description:The Increased Toxicity of UV-Degraded Nitroguanidine and IMX-101 Exposures in Zebrafish Larvae: Evidence Implicating Oxidative Stress [2]

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Lipidomics of GATA1 mutant cells during erythroid maturation

| MSV000092894 | MassIVE