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Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage [RNA-seq]

ABSTRACT: Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage [RNA-seq]

PROVIDER: PRJNA819545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18474132_1.fastq.gz	Fastqsanger.gz
	SRR18474132_2.fastq.gz	Fastqsanger.gz
	SRR18474133_1.fastq.gz	Fastqsanger.gz
	SRR18474133_2.fastq.gz	Fastqsanger.gz
	SRR18474134_1.fastq.gz	Fastqsanger.gz

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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Aflatoxin B1 (AFB1) is amongst the mycotoxins commonly affecting human and animal health, raising global food safety and control concerns. The mechanisms underlying AFB1 toxicity are poorly understood. Moreover, antidotes against AFB1 are lacking. Genome-wide CRISPR/Cas9 knockout screening in porcine kidney cells identified the transcription factor BTB and CNC homolog 1 (BACH1) as a gene required for AFB1 toxicity. The inhibition of BACH1 expression in porcine kidney cells and human hepatoma cells resulted in increased resistance to AFB1. BACH1 depletion attenuates AFB1-induced oxidative damage via the upregulation of antioxidant genes.

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Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage

Project description:Genome-scale CRISPR knockout screen identifies BACH1 as a key regulator of aflatoxin B1-induced oxidative damage

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Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [RNA-seq]

Project description:Explore the potential downstream signaling pathways that resist AFB1 toxicity after knocking out BACH1 by RNA-seq analysis.

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