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RNAseq data from WT and Lbr N-terminal mutant, divided for sex

ABSTRACT: RNAseq data from WT and Lbr N-terminal mutant, divided for sex

PROVIDER: PRJNA694630 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13520810_1.fastq.gz	Fastqsanger.gz
	SRR13520810_2.fastq.gz	Fastqsanger.gz
	SRR13520811_1.fastq.gz	Fastqsanger.gz
	SRR13520811_2.fastq.gz	Fastqsanger.gz
	SRR13520812_1.fastq.gz	Fastqsanger.gz

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RNAseq data from WT and Lbr N-terminal mutant, divided for sex

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The human cholesterogenic enzymes DHCR14 and LBR are differentially regulated transcriptionally and post-translationally

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Project description:The goal of this study was to identify accessible chromatin peaks in lamina-associated domains of senescent cells. To establish senescence we used ionizing radiation (IR), overexpression of miR-340-5p, and knockdown of Lamin B Receptor (LBR).One of the cellular processes influenced by microRNAs is senescence, a state of indefinite growth arrest triggered by sublethal cell damage. Here, through bioinformatic analysis and experimental validation, we identified miR-340-5p as a novel miRNA that foments cellular senescence. miR340-5p was highly abundant in diverse senescence models, and miR-340-5p overexpression in proliferating cells rendered them senescent. Among the target mRNAs, miR-340-5p prominently reduced the levels of LBR mRNA, encoding Lamin B Receptor (LBR). Loss of LBR by ectopic overexpression of miR-340-5p derepressed heterochromatin in lamina-associated domains (LADs), promoting the expression of DNA repetitive elements characteristic of senescence. Importantly, overexpressing miR-340-5p enhanced cellular sensitivity to senolytic compounds, while antagonization of miR-340-5p reduced senescent-cell markers and engendered resistance to senolytic-induced cell death. We propose that miR-340-5p can be exploited for clearing senescent cells to restore tissue homeostasis and mitigate damage by senescent cells in aging human pathologies.

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