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NEIL DNA glycosylase deficient HAP1 cells

ABSTRACT: Enhanced glutathione levels confer resistance to apoptotic and ferroptotic programmed cell death in NEIL DNA glycosylase deficient HAP1 cells

PROVIDER: PRJEB66137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR12511942_1.fastq.gz	Fastqsanger.gz
	ERR12511942_2.fastq.gz	Fastqsanger.gz
	ERR12511943_1.fastq.gz	Fastqsanger.gz
	ERR12511943_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Enhanced glutathione levels confer resistance to apoptotic and ferroptotic programmed cell death in NEIL DNA glycosylase deficient HAP1 cells

Project description:Enhanced glutathione levels confer resistance to apoptotic and ferroptotic programmed cell death in NEIL DNA glycosylase deficient HAP1 cells

| PRJNA1013047 | ENA

Enhanced glutathione levels confer resistance to apoptotic and ferroptotic programmed cell death in NEIL DNA glycosylase deficient HAP1 cells

Project description:The NTHL1 and NEIL1-3 DNA glycosylases are major enzymes in the removal of oxidative DNA base lesions, via the base excision repair (BER) pathway. To investigate their interplay in human cells, we engineered single, double, triple, and quadruple DNA glycosylase deficient HAP1 cells using the Crisp-cas 9 technology. We found that these DNA glycosylase deficient cells are more resistant to oxidative stress caused by genotoxic agents than wild type cells, and a further augment in resistance was observed upon inhibition of glutathione synthesis. Gene expression analysis revealed that GSH depletion activates the NRF2/KEAP1 pathway and ER stress induced apoptosis. Furthermore, glutathione depleted NEIL triple KO cells are also more resistant to cell death induced via ferroptosis than wild type cells. Finally, we observed higher basal level of glutathione and differential expression of NRF2-regulated genes associated with glutathione homeostasis in these cells. We propose that NEIL deficiency leads to aberrant transcription and subsequent errors in protein synthesis, which cause ER- and proteotoxic stress. This triggers the unfolded protein response, which consequently upregulates intracellular antioxidant defence mechanisms. Altogether, our data suggest that NEIL deficient cells developed an oxidative stress defence mechanism termed hormesis mediated by elevated GSH levels in response to the increased intracellular stress inflicted by loss of NEIL123 activities.

2023-09-08 | GSE242290 | GEO

Transcriptome regulated by NEIL2 in human HAP1 cells

Project description:To elucidate the role of DNA glycosylase NEIL2 in transcriptome regulation, we performed RNA sequencing in human HAP1 cells of Neil2 knockout and wild type. The tanscription count was extracted and the differential expressed genes (DEGs) were analysed.

2023-12-13 | GSE240564 | GEO

RNA-seq of human pancreatic cancer cell line PANC-1 treated with RSL-3, N6F11, Fin56 and Erastin against untreated controls

Project description:Ferroptotic cell death is dependent on unrestricted lipid peroxidation rather than activation of apoptotic effector caspases. A large number of ferroptosis activators have been reported recently. We used gene sequencing to analyze the effects of four ferroptosis activators (RSL3, N6F11, Fin56 and Erastin) on global gene expression in human PDAC1 cell line.

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A genome-wide CRISPR screen identifies mediators of ferroptosis sensitivity in polyunsaturated fatty acid-treated cells

Project description:Polyunsaturated fatty acids (PUFA) sensitize cells to ferroptotic cell death. In the study associated with this dataset, we used UACC257 as a model cell line (intrinsically resistant to ferroptosis) induced to be sensitive to ferroptosis with different PUFAs. We performed genome-wide CRISPR knockout screen to identify genes that mediate the sensitivity to ML210, a selective inhibitor of glutathione peroxidase 4 (GPX4) and a potent inducer of ferroptotic cell death. We identified cytochrome P450 oxidoreductase (POR, CYPOR) as a key player required for ferroptotic cell death among other genes.

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Project description:Expression microarray experiments were performed to identify all of the aerobic and hypoxic transcripts in wild-type cells. The role of Hap1 in the regulation of transcription was examined by monitoring gene expression in hap1 deletion cells. Keywords: gene expression, strain comparison, response to hypoxic conditions

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Project description:We analyzed the global change in transcription upon CHD3-KO and SENP1-KO compared to control HAP1 cells.

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