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  The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle

Warnatz, H. J., Schmidt, D., Manke, T., Piccini, I., Sultan, M., Borodina, T., et al. (2011). The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle. The Journal of Biological Chemistry, 286(26), 23521-32. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21555518 http://www.jbc.org/content/286/26/23521.full.pdf.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-78F4-A Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-78F5-8
Genre: Journal Article

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Warnatz, H. J.1, Author              
Schmidt, D., Author
Manke, T.2, Author              
Piccini, I., Author
Sultan, M.1, Author              
Borodina, T.3, Author              
Balzereit, D.1, Author              
Wruck, W., Author
Soldatov, A.3, Author              
Vingron, M.4, Author              
Lehrach, H.5, Author              
Yaspo, M. L.1, Author              
Affiliations:
1Human Chromosome 21 (Marie-Laure Yaspo), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479652              
2Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433547              
3Technology Development(Alexey Soldatov), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479657              
4Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479639              
5Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              

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Free keywords: Basic-Leucine Zipper Transcription Factors/genetics/*metabolism; Cell Cycle/*physiology; Fanconi Anemia Complementation Group Proteins/genetics/*metabolism; Gene Expression Profiling; Gene Expression Regulation/*physiology; HEK293 Cells; Humans; Oligonucleotide Array Sequence Analysis; Oxidative Stress/*physiology; Response Elements/physiology
 Abstract: The regulation of gene expression in response to environmental signals and metabolic imbalances is a key step in maintaining cellular homeostasis. BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAF recognition elements, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation sequencing analysis of BACH1 target genes in HEK 293 cells with knockdown of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by chromatin immunoprecipitation sequencing were found highly enriched in genes showing expression changes after BACH1 knockdown, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, and SLC48A1) and redox regulation (GCLC, GCLM, and SLC7A11), we also discovered BACH1 target genes affecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, and MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, and 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.

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 Dates: 2011
 Publication Status: Published in print
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Title: The Journal of Biological Chemistry
Source Genre: Journal
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Pages: - Volume / Issue: 286 (26) Sequence Number: - Start / End Page: 23521 - 32 Identifier: ISSN: 1083-351X (Electronic) 0021-9258 (Linking)