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Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

ABSTRACT: Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

PROVIDER: PRJNA1001317 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25491764.fastq.gz	Fastqsanger.gz
	SRR25491765.fastq.gz	Fastqsanger.gz
	SRR25491766.fastq.gz	Fastqsanger.gz
	SRR25491767.fastq.gz	Fastqsanger.gz
	SRR25491768.fastq.gz	Fastqsanger.gz

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Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

Project description:Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

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Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

Project description:EZH2 is a histone methyltransferase that deposits the repressive histone H3 lysine 27 trimethylation (H3K27me3). This mark has been reported to silence expression of various repetitive elements in the genome. We sought to identify the effect of EZH2 inhibition on coding and non-coding, repetitive RNA expression. We generated a novel mutant mouse line whose ability to detect induced repeat element expression has been abrogated. We report that the mutant splenic B cells fail to upregulate inflammatory gene expression upon EZH2 inhibition, despite comparable upregulation of various repetitive elements with WT. Unlike WT splenic B cells that do not upregulate interferon gene expression upon EZH2 inhibition, B16-F10 melanoma cells activate their expression under the same inhibitor treatment. Cytosolic pattern recognition receptors, RIG-I and Cgas, are required for such response as their deletion abrogates this pathway.

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Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

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Treatment of non-CML CD34+ cells with EZH2 inhibitor GSK343

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Project description:Our previous study has found that GSK343 is a potent autophagy inducer. To further investigate the underlying mechanisms, microarray analysis was performed.

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