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Genome-wide analysis of ATF4 binding in histidinol-treated cells and RNA-Seq experiment to identify genes regulated by ATF4

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69309 | GEO | 2015/08/28

SECONDARY ACCESSION(S): PRJNA285115

REPOSITORIES: GEO

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Genome-wide analysis of ATF4 binding in histidinol-treated cells and RNA-Seq experiment to identify genes regulated by ATF4

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-28 | E-GEOD-69309 | biostudies-arrayexpress

RNA-Seq experiment to identify genes regulated by ATF4

2015-08-28 | GSE69308 | GEO

Genome-wide analysis of ATF4 binding in histidinol-treated cells and RNA-Seq experiment to identify genes regulated by ATF4

Project description:Genome-wide analysis of ATF4 binding in histidinol-treated cells and RNA-Seq experiment to identify genes regulated by ATF4

| PRJNA285115 | ENA

RNA-Seq experiment to identify genes regulated by ATF4

Project description:Activating Transcription Factor 4 (ATF4) is a transcription factor induced by the integrated stress response (ISR). This experiment is a genome-wide profiling of ATF4-dependent RNA expression in human HAP-1 cells. HAP-1 is a near-haploid human cell line that was derived from KBM-7 cells isolated from a patient with Chronic Myelogenous Leukemia. We analyzed WT and ATF4 KO cells. We induced ATF4 expression by mimicking amino acid starvation with the drug histidinol. RNA expression profiles were generated for WT and ATF4 KO HAP1 cells. ATF4 genes were mutated using Cas9 genome editing technology. Amino acid starvation was mimicked by treating WT and ATF4 KO cells with 2 mM histidinol for 24 hours, which increases ATF4 expression.

2015-08-28 | E-GEOD-69308 | biostudies-arrayexpress

Genome-wide analysis of ATF4 binding in histidinol-treated cells

2015-08-28 | GSE69304 | GEO

Genome-wide analysis of ATF4 binding in histidinol-treated cells

Project description:Activating Transcription Factor 4 (ATF4) is a transcription factor induced by the integrated stress response (ISR). This experiment is a genome-wide occupancy profiling of ATF4 in human HAP1 cells. HAP1 is a near-haploid human cell line that was derived from KBM-7 cells isolated from a patient with Chronic Myelogenous Leukemia. We induced ATF4 expression by mimicking amino acid starvation with the drug histidinol. We identified peaks of ATF4 binding using three independent antibodies. Examination of ATF4 binding in HAP1 cells treated with 2 mM histidinol for 24 hours.

2015-08-28 | E-GEOD-69304 | biostudies-arrayexpress

Genome wide screens in yeast to identify potential binding sites and target genes of DNA-binding proteins.

Project description:Knowledge of all binding sites for transcriptional activators and repressors is essential for computationally aided identification of transcriptional networks. The techniques developed for defining the binding sites of transcription factors tend to be cumbersome and not adaptable to high throughput. We refined a versatile yeast strategy to rapidly and efficiently identify genomic targets of DNA-binding proteins. Yeast expressing a transcription factor is mated to yeast containing a library of genomic fragments cloned upstream of the reporter gene URA3. DNA fragments with target-binding sites are identified by growth of yeast clones in media lacking uracil. The experimental approach was validated with the tumor suppressor protein p53 and the forkhead protein FoxI1 using genomic libraries for zebrafish and mouse generated by shotgun cloning of short genomic fragments. Computational analysis of the genomic fragments recapitulated the published consensus-binding site for each protein. Identified fragments were mapped to identify the genomic context of each binding site. Our yeast screening strategy, combined with bioinformatics approaches, will allow both detailed and high-throughput characterization of transcription factors, scalable to the analysis of all putative DNA-binding proteins.

| S-EPMC2248728 | biostudies-literature

Genome-wide analysis of HOXC4 and HOXC6 regulated genes and binding sites in prostate cancer cells.

Project description:Aberrant expression of HOXC6 and HOXC4 is commonly detected in prostate cancer. The high expression of these transcription factors is associated with aggressive prostate cancer and can predict cancer recurrence after treatment. Thus, HOXC4 and HOXC6 are clinically relevant biomarkers of aggressive prostate cancer. However, the molecular mechanisms by which these HOXC genes contribute to prostate cancer is not yet understood. To begin to address the role of HOXC4 and HOXC6 in prostate cancer, we performed RNA-seq analyses before and after siRNA-mediated knockdown of HOXC4 and/or HOXC6 and also performed ChIP-seq to identify genomic binding sites for both of these transcription factors. Our studies demonstrate that HOXC4 and HOXC6 co-localize with HOXB13, FOXA1 and AR, three transcription factors previously shown to contribute to the development of prostate cancer. We suggest that the aberrantly upregulated HOXC4 and HOXC6 proteins may compete with HOXB13 for binding sites, thus altering the prostate transcriptome. This competition model may be applicable to many different human cancers that display increased expression of a HOX transcription factor.

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Genome-wide characterization of light-regulated genes in Neurospora crassa.

Project description:The filamentous fungus Neurospora crassa responds to light in complex ways. To thoroughly study the transcriptional response of this organism to light, RNA-seq was used to analyze capped and polyadenylated mRNA prepared from mycelium grown for 24 hr in the dark and then exposed to light for 0 (control) 15, 60, 120, and 240 min. More than three-quarters of all defined protein coding genes (79%) were expressed in these cells. The increased sensitivity of RNA-seq compared with previous microarray studies revealed that the RNA levels for 31% of expressed genes were affected two-fold or more by exposure to light. Additionally, a large class of mRNAs, enriched for transcripts specifying products involved in rRNA metabolism, showed decreased expression in response to light, indicating a heretofore undocumented effect of light on this pathway. Based on measured changes in mRNA levels, light generally increases cellular metabolism and at the same time causes significant oxidative stress to the organism. To deal with this stress, protective photopigments are made, antioxidants are produced, and genes involved in ribosome biogenesis are transiently repressed.

| S-EPMC4169166 | biostudies-literature

Genome-wide studies identify genes directly regulated by PML/RARα fusion protein

Project description:Acute promyelocytic leukemia (APL) is characterized by a specific t(15;17) chromosome translocation that generates the promyelocytic leukemia/retinoic acid receptor-α (PML/RARα) fusion gene. However, the global association between PML/RARα and transcriptional co-regulators, and the rules of their association in governing the key processes during the leukemogenesis remain obscure. Here, we performed the genome-wide binding profiling of PML/RARα, HDAC1 and P300, in NB4, an APL patient-derived cell line. We found that PML/RARα targets could be classified into two classes. Moreover, we also performed ChIP-seq of H3K27ac to determine super-enhancers in NB4. We identified a novel function of PML/RARα in super-enhancer regulation during the leukemogenesis of APL.

2020-08-26 | GSE126720 | GEO

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