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RNA-Seq experiment to identify genes regulated by ATF4

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69308 | GEO | 2015/08/28

SECONDARY ACCESSION(S): PRJNA285117

REPOSITORIES: GEO

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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

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 analysis of ATF4 binding in histidinol-treated cells

2015-08-28 | GSE69304 | GEO

RNAseq Analysis of TP53+/+ and TP53-/- HCT116 colon carcinoma cell lines after treatment with p53 or ATF4-activating compounds

Project description:We examined the gene expression changes resulting from treatment of either "wild-type" or "p53-deficient" human cell lines with compounds known to activate either p53 (nutlin-3A,etoposide) or the integrated stress response (ISR) transcription factor ATF4 (histidinol,tunicamycin)

2022-08-20 | GSE211244 | GEO

ISR target genes revealed by comprehensive microarray network study using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK

Project description:To identify the target genes of integrated stress reponse (ISR), we have employed whole genome microarray expression in MEF cells. ISR gene setimation under ER stress condition using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK MEF cells

2015-09-01 | E-GEOD-49598 | biostudies-arrayexpress

Microarray expression data of NCI-H1975 cells treated with osimertinib, alpelisib, or combination of these in the presence or absence of L-histidinol.

Project description:Oncogenic signals often activate abnormal proliferation, while simultaneously activate stress-adaptive mechanisms such as the integrated stress response (ISR) to ensure rapid growth under intrinsic and extrinsic stress conditions. In this study, we investigated the involvement of EGFR-PI3K pathway in the regulation of ISR in EGFR-mutant NSCLC cell lines under amino acid deprivation. We found that the third generation EGFR inhibitor osiemrtinib suppressed induction of activation transcription factor 4 (ATF4), the key ISR effector, in EGFR mutant cells, while the effect was to a less extent in cells harboring PIK3CA-co-alteration. PI3K inhibitors including P110a-specific inhibitor alpelicib markedly suppress ATF4 induction in PIK3CA-mutant cell lines. To further explore the role of EGFR-PI3K, transcriptome analysis was performed in EGFR- and PIK3CA-mutated NCI-H1975 cells treated with osimertinib, alpelisib, or combination of these in the absence or presence of histidyl-tRNA inhibitor L-histidinol (His), mimicking amino acid deprived conditions. Among His-induced genes, either osimertinib or alpelisib partially, but the combination dramatically suppressed a cluster of genes targeted by ATF4. Furthermore, combination of osimertinib and alpelisib increased apoptotic cells under amino acid deprived conditions. These results indicate that oncogenic EGFR-PI3K pathway contributes to cellular adaptation to stress conditions through ATF4. We used microarrays to identify genes whose expression is up- or down-regulated by inhibition of EGFR, PI3K, or both under amino acid deprivation.

2023-03-22 | GSE216508 | GEO

Cut&Run Analysis of ATF4 genomic occupancy in HCT116 colon carcinoma cell lines after treatment with DMSO, etoposide, tunicamycin, or histidinol

Project description:We examined ATF4 genomic occupancy resulting from treatment of HCT116 colon carcinoma human cell lines with DMSO, etoposide, histidinol, or, tunicamycin, using Cut&Run.

2022-08-20 | GSE211264 | GEO

Activation of ISR/ATF4 signaling depletes HIV reservoir in CD4+ T cells

Project description:Latent HIV reservoirs are extremely stable which pose a tremendous challenge to eradicate HIV. Here, we show that HIV explores the integrated stress response (ISR) signaling to establish its quiescent infection, refractory to the clearance for its persistence. HA15, a recently characterized specific ISR agonist, activates ATF4/CHOP signaling to not only disrupt HIV latency but also reduce HIV+ cells in the primary CD4+ T cell model of HIV latency without the induction of cell death in the HIV negative primary CD4+ T cells and the impact of viability in resting CD4+ T cells isolated from people living with HIV (PLWH). Mechanistically, the reduction of HIV+ cells by ISR/ATF4 activation is associated with the enhancement of cellular apoptosis. However, this mainly occurs in the HIV translation negative CD4+ T cells. In fact, ISR/ATF4 activation-induced cell death largely occurs in HIV transcription active (HIV gag-pol) CD4+ T cells. This is involved in HIV RNA-induced innate immune IFIT signaling. During the acute SIV infection in the rhesus macaques, the induction of ATF4 is associated with decrease of SIV reservoir in the intestine in vivo. When further tested in the resting CD4+ T cells isolated from PLWH on ART, the induction of ISR/ATF4 signaling by HA15 reduced HIV DNA reservoir. These findings support that inactivation of ISR/ATF4 signaling is associated with the maintenance of the stable and quiescent HIV reservoirs while enforced ISR/ATF4 signaling reduces translation quiescent HIV reservoirs in CD4+ T cells.

2022-12-05 | GSE210824 | GEO

Genome wide binding of ATF4 and CEBPG bZIP transcription factors in MEFs under amino acid deprived (AAD) conditions

Project description:The integrated stress response (ISR) controls cellular adaptations to nutrient deprivation, redox imbalances and ER stress. ISR genes are upregulated in stressed cells, primarily by the bZIP transcription factor ATF4 through its recruitment to cis-regulatory C/EBP:ATF response elements (CAREs) together with a dimeric partner of uncertain identity. Here we show that C/EBPÎ³:ATF4 heterodimers, but not C/EBPÎ²:ATF4 dimers, are the predominant CARE binding species in stressed cells. C/EBPÎ³ and ATF4 associate with genomic CAREs in a mutually-dependent manner and co-regulate many ISR genes. By contrast, the C/EBP family members C/EBPÎ² and CHOP were largely dispensable for induction of stress genes. Cebpgâ/â MEFs proliferate poorly and exhibit oxidative stress due to reduced glutathione levels and impaired expression of several glutathione biosynthesis pathway genes. Cebpgâ/â mice (C57BL/6 background) display reduced body size and microphthalmia, similar to ATF4-null animals. In addition, C/EBPÎ³-deficient newborns die from atelectasis and respiratory failure which can be mitigated by in utero exposure to the anti-oxidant, N-acetyl-cysteine. Cebpgâ/â mice on a mixed strain background show improved viability but, upon aging, develop significantly fewer malignant solid tumors compared to WT animals. Our findings identify C/EBPÎ³ as a novel anti-oxidant regulator and an obligatory ATF4 partner that controls redox homeostasis in normal and cancerous cells. Evaluation of genomic binding of 2 bZIP transcription factors under amino acid deprivation conditions in mouse embryonic fibroblasts

2015-11-19 | E-GEOD-75165 | biostudies-arrayexpress

Whole genome expression data from WT, Atf4-/-, and Cebpg-/- MEFs under normal and amino acid deprived (AAD) growth conditions

Project description:The integrated stress response (ISR) controls cellular adaptations to nutrient deprivation, redox imbalances and ER stress. ISR genes are upregulated in stressed cells, primarily by the bZIP transcription factor ATF4 through its recruitment to cis-regulatory C/EBP:ATF response elements (CAREs) together with a dimeric partner of uncertain identity. Here we show that C/EBPÎ³:ATF4 heterodimers, but not C/EBPÎ²:ATF4 dimers, are the predominant CARE binding species in stressed cells. C/EBPÎ³ and ATF4 associate with genomic CAREs in a mutually-dependent manner and co-regulate many ISR genes. By contrast, the C/EBP family members C/EBPÎ² and CHOP were largely dispensable for induction of stress genes. Cebpgâ??/â?? MEFs proliferate poorly and exhibit oxidative stress due to reduced glutathione levels and impaired expression of several glutathione biosynthesis pathway genes. Cebpgâ??/â?? mice (C57BL/6 background) display reduced body size and microphthalmia, similar to ATF4-null animals. In addition, C/EBPÎ³-deficient newborns die from atelectasis and respiratory failure which can be mitigated by in utero exposure to the anti-oxidant, N-acetyl-cysteine. Cebpgâ??/â?? mice on a mixed strain background show improved viability but, upon aging, develop significantly fewer malignant solid tumors compared to WT animals. Our findings identify C/EBPÎ³ as a novel anti-oxidant regulator and an obligatory ATF4 partner that controls redox homeostasis in normal and cancerous cells. WT, Atf4-/-, and Cebpg-/- MEFs (passage 3) were cultured under normal and AAD conditions. RNA from each treatment condition was collected in triplicate for hybrization on Affymetrix Mouse Genome 430 2.0 microarrays.

2015-11-19 | E-GEOD-75150 | biostudies-arrayexpress

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