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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

ABSTRACT: BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

PROVIDER: PRJNA695525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13571564.fastq.gz	Fastqsanger.gz
	SRR13571565.fastq.gz	Fastqsanger.gz
	SRR13571566.fastq.gz	Fastqsanger.gz
	SRR13571567.fastq.gz	Fastqsanger.gz
	SRR13571568.fastq.gz	Fastqsanger.gz

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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

Project description:The cystic fibrosis transmembrane conductance regulator (CFTR) gene lies within a TAD in which multiple cis-regulatory elements (CREs) and transcription factors (TFs) regulate its cell-specific expression. The CREs are recruited to the gene promoter by a looping mechanism that depends upon both architectural proteins and specific TFs. An siRNA screen to identify TFs coordinating CFTR expression in airway epithelial cells suggested an activating role for BTB Domain and CNC Homolog 1 (BACH1). BACH1 is a ubiquitous master regulator of the cellular response to oxidative stress. Here we show that BACH1 may have a dual effect on CFTR expression by direct occupancy of CREs at physiological oxygen (~8%), while indirectly modulating expression under conditions of oxidative stress. Hence BACH1, can activate or repress the same gene, to fine tune expression in response to environmental cues such as cell stress. Furthermore, our 4C-seq data suggest that BACH1 can also directly regulate CFTR gene expression by modulating locus architecture through occupancy at known enhancers and structural elements, and depletion of BACH1 alters the higher order chromatin structure.

2021-11-17 | GSE165717 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

2021-11-17 | GSE165718 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

| PRJNA695530 | ENA

BACH1 as a master regulator gene in vascular cells during aging

Project description:We identify transcription factor BACH1 as a master regulator in vascular cells during aging. BACH1 is upregulated in the aorta of old mice. We find BACH1 is located on open chromatin and BACH1 binds to CDKN1A gene enhancer and activates its transcription in endothelial cells. Finally, BACH1 aggravates endothelial cell senescence under oxidative stress. Thus, these findings demonstrate a crucial regulatory role of BACH1 in vascular aging.

2024-09-15 | GSE185210 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

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

2021-11-17 | GSE165719 | GEO

BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression.

Project description:The cystic fibrosis transmembrane conductance regulator (CFTR) gene lies within a topologically associated domain (TAD) in which multiple cis-regulatory elements (CREs) and transcription factors (TFs) regulate its cell-specific expression. The CREs are recruited to the gene promoter by a looping mechanism that depends upon both architectural proteins and specific TFs. An siRNA screen to identify TFs coordinating CFTR expression in airway epithelial cells suggested an activating role for BTB domain and CNC homolog 1 (BACH1). BACH1 is a ubiquitous master regulator of the cellular response to oxidative stress. Here, we show that BACH1 may have a dual effect on CFTR expression by direct occupancy of CREs at physiological oxygen (∼8%), while indirectly modulating expression under conditions of oxidative stress. Hence BACH1, can activate or repress the same gene, to fine tune expression in response to environmental cues such as cell stress. Furthermore, our 4C-seq data suggest that BACH1 can also directly regulate CFTR gene expression by modulating locus architecture through occupancy at known enhancers and structural elements, and depletion of BACH1 alters the higher order chromatin structure.

| S-EPMC8589331 | biostudies-literature

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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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