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Project description:Maintenance of genetic integrity is essential for survival of all organisms. Activating transcription factor 3 (ATF3) is a member of the c-AMP response element binding (CREB)/ATF family of transcription factors, and is highly inducible by various stress conditions including DNA damage. However, downstream targets and molecular basis underlying pleiotropic effects of ATF3 on the cell fate have been largely unknown. To identify ATF3 targets in the human genome, we carried out chromatin immunoprecipitation-microarray (ChiP-on-chip) and knockdown-expression profiling analysis using two models where ATF3 was either transiently induced or constitutively expressed. We show that ATF3 binds to an unexpectedly large number of targets; 5,984 promoters in HCT116 cells treated with an alkylating agene methyl methanesulfonate (MMS) and 1,423 promoters in LNCaP cells constitutively expressing ATF3. Importantly, targets of MMS-induced ATF3 are highly enriched not only for CREB/ATF motifs but also for binding sites of several stress sensors including DDIT3/CHOP, Egr1, and c-Ets which are concomitantly induced by MMS. Stress-induced ATF3 affects broad but select biological processes including cell cycle, cell death, adhesion, biosynthesis, and receptor signaling pathways. In addition, ATF3 binds to as many as 40% of the p53 targets and preferentially enhances MMS-induced activation of proapoptotic genes such as DR4, DR5, and PUMA, consistent with the proapoptotic effect of ATF3. These data shed new light on the co-regulatory function of ATF3 in the stress-induced transcription factor network. The comprehensive list of genomic targets of ATF3 will facilitate further understanding the role of ATF3 in determining life and death of cells under both physiological and tumour-associated stress conditions. Maintenance of genetic integrity is fundamental to survival of all organisms. DNA damage can be caused by various agents in environment and elicits complex responses in the cell. ATF3 is one of the transcription factors activated by various stress conditions including DNA damage, and has been shown to have pleiotropic effects on life and death of cells depending on the context of experimental conditions. It has been largely unknown, however, which genes and pathways are regulated by stress-induced ATF3. Here we attempted to answer this question by chromatin immunoprecipitation-microarray analysis of downstream targets of ATF3. We show that ATF3 binds to an unexpectedly large number of promoters (nearly 6,000) in a human colorectal cancer cell lineHCT116 treated with an alkylating agent methyl methanesulfonate. Interestingly, the ATF3 targets are highly enriched for binding sites of other stress sensors shedding light on a transcriptional co-regulatory network of DNA damage response. We further show that ATF3 regulates expression of genes in select biological processes including cell cycle, cell death, adhesion, metabolism, signal transduction, and the p53 pathway. The comprehensive list of ATF3 targets provides new insight into a highly inter-connected network of stress-induced transcription factors around ATF3. ChIP-chip samples: Comparison of ATF3-IP and whole genome DNA (control) Gene expression samples: HCT116 cells pre-transfected with either control siRNA or ATF3 knockdown siRNA and stimulated by methyl methanesulfonate (MMS) for 0, 6, 12, and 24 hours
2010-10-01 | E-GEOD-18457 | biostudies-arrayexpress
Project description:H2B binding profiling analysis of ChIP-seq data for WT and ATF3-iKO satellite cells
2022-06-06 | GSE205324 | GEO
Project description:The submitted files contain ChIP-seq data for the MyoD and myogenin muscle regulatory factors in diffrentiated C2C12 cells as well as two different sonicated input samples (one from a regular 1% formaldehyde fixation and one from a dual 1%FA + 1.5 mM EGS fix). Characterization of genome-wide MyoD and myogenin binding in C2C12 cells
2013-06-01 | E-GEOD-44824 | biostudies-arrayexpress
Project description:Maintenance of genetic integrity is essential for survival of all organisms. Activating transcription factor 3 (ATF3) is a member of the c-AMP response element binding (CREB)/ATF family of transcription factors, and is highly inducible by various stress conditions including DNA damage. However, downstream targets and molecular basis underlying pleiotropic effects of ATF3 on the cell fate have been largely unknown. To identify ATF3 targets in the human genome, we carried out chromatin immunoprecipitation-microarray (ChiP-on-chip) and knockdown-expression profiling analysis using two models where ATF3 was either transiently induced or constitutively expressed. We show that ATF3 binds to an unexpectedly large number of targets; 5,984 promoters in HCT116 cells treated with an alkylating agene methyl methanesulfonate (MMS) and 1,423 promoters in LNCaP cells constitutively expressing ATF3. Importantly, targets of MMS-induced ATF3 are highly enriched not only for CREB/ATF motifs but also for binding sites of several stress sensors including DDIT3/CHOP, Egr1, and c-Ets which are concomitantly induced by MMS. Stress-induced ATF3 affects broad but select biological processes including cell cycle, cell death, adhesion, biosynthesis, and receptor signaling pathways. In addition, ATF3 binds to as many as 40% of the p53 targets and preferentially enhances MMS-induced activation of proapoptotic genes such as DR4, DR5, and PUMA, consistent with the proapoptotic effect of ATF3. These data shed new light on the co-regulatory function of ATF3 in the stress-induced transcription factor network. The comprehensive list of genomic targets of ATF3 will facilitate further understanding the role of ATF3 in determining life and death of cells under both physiological and tumour-associated stress conditions. Maintenance of genetic integrity is fundamental to survival of all organisms. DNA damage can be caused by various agents in environment and elicits complex responses in the cell. ATF3 is one of the transcription factors activated by various stress conditions including DNA damage, and has been shown to have pleiotropic effects on life and death of cells depending on the context of experimental conditions. It has been largely unknown, however, which genes and pathways are regulated by stress-induced ATF3. Here we attempted to answer this question by chromatin immunoprecipitation-microarray analysis of downstream targets of ATF3. We show that ATF3 binds to an unexpectedly large number of promoters (nearly 6,000) in a human colorectal cancer cell lineHCT116 treated with an alkylating agent methyl methanesulfonate. Interestingly, the ATF3 targets are highly enriched for binding sites of other stress sensors shedding light on a transcriptional co-regulatory network of DNA damage response. We further show that ATF3 regulates expression of genes in select biological processes including cell cycle, cell death, adhesion, metabolism, signal transduction, and the p53 pathway. The comprehensive list of ATF3 targets provides new insight into a highly inter-connected network of stress-induced transcription factors around ATF3.
2010-10-01 | GSE18457 | GEO
Project description:ATF3 binding sites on the genome and histone modification arround the ATF3 binding sites were analized by ChIP-seq. Regulation of gene expression by ATF3 on active enhacer regions were analyzed by knocked down of ATF3.
2020-05-26 | GSE141385 | GEO
Project description:In this study, we used ChIP-seq to map Six4 binding profile in different C2C12 cell lines 24 hours after differentiation (T24). We performed ChIP-seq using two different antibodies: anti-Flag antibody in Flag-Six4 C2C12 cell line or in parental C2C12 cells; a custom-made anti-Six4 antibody in shNS C2C12 cell line (a control cell line) or shSix4 C2C12 (C2C12 with stable Six4 knockdown using short hairpin RNA). We also performed ChIP-seq in parental C2C12 cells using normal rabbit IgG. We were able to identify Six4-bound loci in C2C12 T24 that were recognized by two different antibodies and showed a decrease in peak intensity in shSix4 C2C12 compared to shNS C2C12 cells.
2015-12-31 | GSE66901 | GEO
Project description:In this study, we used ChIP-seq to map Six4 binding profile in different C2C12 cell lines 24 hours after differentiation (T24). We performed ChIP-seq using two different antibodies: anti-Flag antibody in Flag-Six4 C2C12 cell line or in parental C2C12 cells; a custom-made anti-Six4 antibody in shNS C2C12 cell line (a control cell line) or shSix4 C2C12 (C2C12 with stable Six4 knockdown using short hairpin RNA). We also performed ChIP-seq in parental C2C12 cells using normal rabbit IgG. We were able to identify Six4-bound loci in C2C12 T24 that were recognized by two different antibodies and showed a decrease in peak intensity in shSix4 C2C12 compared to shNS C2C12 cells. We established a C2C12 cell line with stable Six4 knockdown by short hairpin RNA (shSix4) vs. a control cell line (shNS). We also established a C2C12 cell line with stable expression of Flag-Six4-myc by infection of retroviruses expressing pBABE-Flag-Six4-myc (Flag-Six4 C2C12) vs. parental C2C12. We differentiate these cells for 24 hours before using them for ChIP-seq.
2015-12-31 | E-GEOD-66901 | biostudies-arrayexpress
Project description:ChIP-seq for TAZ (WWTR1) binding region in C2C12 myoblasts
| PRJEB26667 | ENA
Project description:We demonstrated that TAZ positively regulates Irs1 gene transcription in muscle. Therefore we designed ChIP-seq experiment to reveal detailed mechanism of regulation. To capture TAZ in chromatin preparation, we made Flag-tagged TAZ expressing and control vector transduced C2C12 cells by retroviral infection. We used FLAG-conjugated beads to capture TAZ-chromatin complexes and ChIP-seq was perforemd. Among many TAZ binding sites, we focused Irs1 regulatory region because our primary purpose was to identify TAZ binding site for the regulation of Irs1 transcription.
2018-12-13 | E-MTAB-6764 | biostudies-arrayexpress