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Expression data from wild type and Bach1 knock out ventral mid brains of two month old mice.

ABSTRACT: Bach1 is a known repressor of NRF2 transcription factor which governs oxidative stress during pathophysiology of Parkinson's disease. NRF2 activation in ventral midbrain is associated with protection against oxidative stress induced apoptosis of DA neurons. In this study we hve evaluated the effect of loss of Bach1 fucntion in ventral mid brains.

ORGANISM(S): Mus musculus

PROVIDER: GSE164412 | GEO | 2021/12/29

REPOSITORIES: GEO

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Expression data from wild type and Bach1 knock out ventral mid brains of two month old mice.

Project description:Expression data from wild type and Bach1 knock out ventral mid brains of two month old mice.

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Genome-wide map of BACH1 binding in HEK 293T cells

Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.

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