ChIP sequencing of BACH1 in mTC and mTN cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA526678 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8714660.fastq.gz | Fastqsanger.gz | |||
| SRR8714661.fastq.gz | Fastqsanger.gz | |||
| SRR8714662.fastq.gz | Fastqsanger.gz | |||
| SRR8714663.fastq.gz | Fastqsanger.gz | |||
| SRR8714664.fastq.gz | Fastqsanger.gz |
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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.
2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress
Project description:The goal of the study is to define the impact of long-term administration of antioxidants on lung cancer progression. mTC and mTN cell lines were established from mice with KrasG12D/+ lung tumors 58 weeks post intranasal Cre-delivery. mTC cells comes from control mice, mTN cells come from NAC-treated mice. Mice were maintained on a mixed C57BL/6-129/Sv genetic background
2019-07-02 | GSE128180 | GEO
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.
2011-05-13 | GSE28051 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE28050: Expression data from knockdown of BACH1 in HEK 293T cells GSE28051: Genome-wide map of BACH1 binding in HEK293T cells Refer to individual Series
2011-05-12 | E-GEOD-28053 | biostudies-arrayexpress
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
Project description:BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1 directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression.
2019-12-18 | GSE124406 | GEO
Project description:The transcription factor BACH1 is a master regulator of human breast cancer metastasis. Here we use gene expression array analysis to identify and compare the genes regulated by BACH1 depletion in a metastatic human breast cancer cell line. Total RNAs were extracted from vector control 1833 cells or 1833 cells with shBACH mRNA BACH1 depletion. Affymetrix GeneChip Human Gene 1.0 ST Arrays were performed to detail the gene expression and identify the genes regulated by BACH1in metastatic human breast cancer cells.
2013-10-31 | E-GEOD-50226 | biostudies-arrayexpress
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
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 performed knock-down of BACH1 in HEK 293T cells using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. Knockdown of BACH1 in HEK 293T cells was carried out with three different types of siRNA molecules (esiRNA = e, siRNA1 SI00309876 from Qiagen = q and Stealth siRNA2 HSS100910 from Invitrogen = s), followed by RNA extraction after 24h and 72h of knockdown and hybridization on Affymetrix microarrays. For each siRNA type, we performed the experiments in triplicates, with four control replicates (mock transfections without siRNA) at 24h and three control replicates at 72h, resulting in nine samples and four controls at 24h and nine samples and three controls at 72h. Samples at 24h of knockdown: e_1_24, e_2_24, e_3_24, q_1_24, q_2_24, q_3_24, s_1_24, s_2_24, s_3_24. Controls at 24h: m_1_24, m_2_24, m_3_24, m_4_72. Samples at 72h of knockdown: e_1_72, e_2_72, e_3_72, q_1_72, q_2_72, q_3_72, s_1_72, s_2_72, s_3_72. Controls at 72h: m_1_72, m_2_72, m_3_72. REPEATS: biological replicate: BACH1_e_1_24, BACH1_e_2_24, BACH1_e_3_24 biological replicate: BACH1_q_1_24, BACH1_q_2_24, BACH1_q_3_24 biological replicate: BACH1_s_1_24, BACH1_s_2_24, BACH1_s_3_24 biological replicate: BACH1_m_1_24, BACH1_m_2_24, BACH1_m_3_24, BACH1_m_4_24 biological replicate: BACH1_e_1_72, BACH1_e_2_72, BACH1_e_3_72 biological replicate: BACH1_q_1_72, BACH1_q_2_72, BACH1_q_3_72 biological replicate: BACH1_s_1_72, BACH1_s_2_72, BACH1_s_3_72 biological replicate: BACH1_m_1_72, BACH1_m_2_72, BACH1_m_3_72
2011-05-13 | E-GEOD-28050 | biostudies-arrayexpress
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 performed knock-down of BACH1 in HEK 293T cells using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays.
2011-05-13 | GSE28050 | GEO