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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

ABSTRACT: Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

PROVIDER: PRJNA623289 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11472100_1.fastq.gz	Fastqsanger.gz
	SRR11472100_2.fastq.gz	Fastqsanger.gz
	SRR11472101_1.fastq.gz	Fastqsanger.gz
	SRR11472101_2.fastq.gz	Fastqsanger.gz
	SRR11472102_1.fastq.gz	Fastqsanger.gz

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

Project description:Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [HMCP-Seq]

Project description:Using bisulfite padlock probes, mRNA sequencing, and hydroxymethylcytosine pull-down sequencing, we show that TET2 loss particularly influences DNA methylation (5mC) and hydroxymethylation (5hmC) patterns at erythroid gene enhancers and is associated with down-regulation of erythroid gene expression in the human erythroleukemia cell line TF-1. We show that 5-Aza disproportionately induces expression of these down regulated genes in TET2KO cells and that this effect may be related to 5mC changes at erythroid gene enhancers after 5-Aza exposure. This work highlights the role of 5mC and 5hmC changes at distal regulatory elements in regulating the expression of differentiation-associated gene signatures, and sheds light on how 5-Aza may be more effective in patients harboring TET2 mutations.

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [Bisulfite-seq]

2020-10-26 | GSE148012 | GEO

Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells [RNA-seq]

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Dysregulated erythroid gene expression after TET2 loss is partially corrected by 5-azacytidine in TF-1 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-26 | GSE148120 | GEO

Desulfuromonas sp. TF strain:TF

Project description:Desulfuromonas sp. TF strain:TF Genome sequencing and assembly

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The dysregulated <i>Pink1<sup>-</sup> Drosophila</i> mitochondrial proteome is partially corrected with exercise.

Project description:One of the genes which has been linked to the onset of juvenile/early onset Parkinson's disease (PD) is PINK1. There is evidence that supports the therapeutic potential of exercise in the alleviation of PD symptoms. It is possible that exercise may enhance synaptic plasticity, protect against neuro-inflammation and modulate L-Dopa regulated signalling pathways. We explored the effects of exercise on Pink1 deficient Drosophila melanogaster which undergo neurodegeneration and muscle degeneration. We used a 'power-tower' type exercise platform to deliver exercise activity to Pink1- and age matched wild-type Drosophila. Mitochondrial proteomic profiles responding to exercise were obtained. Of the 516 proteins identified, 105 proteins had different levels between Pink1- and wild-type non-exercised Drosophila. Gene ontology enrichment analysis and STRING network analysis highlighted proteins and pathways with altered expression within the mitochondrial proteome. Comparison of the Pink1- exercised proteome to wild-type proteomes showed that exercising the Pink1- Drosophila caused their proteomic profile to return towards wild-type levels.

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Project description:Adrenocortical carcinomas (ACCs) are rare and aggressive endocrine cancers of the adrenal gland. Recently, a subtype of ACC characterized by a CpG island methylator phenotype (CIMP), associated with especially poor diagnosis, has been discovered. The purpose of this study is to investigate the role of DNA methylation and the impact on demethylating agent 5-azacytidine in ACC tumors aggressiveness. To this aim, we generated RRBS and RNAseq data from two ACC and one non-tumour cell lines treated or not with 5-azacytidine. We showed that CIMP has a direct impact on the aggressiveness of tumors through two main mechanisms; (1) by increasing survival and proliferation and (2) by favoring the tumor immune escape. These two mechanisms could at least partially be reversed upon 5-azacytidine treatment. Overall, our results show that strongly suggest that the co-treatment with demethylating agents to enhance the efficacy of immunotherapy could be beneficial for patients with high CIMP ACC.

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