AICAR regulate IEGs expression in ALL cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE152917 | GEO | 2021/07/22
REPOSITORIES: GEO
Similar Datasets
Project description:AICAR regulate IEGs expression in ALL cells
| PRJNA640928 | ENA
Project description:AICAR monophosphate (5-Aminoimidazole-4-carboxamide ribonucleotide) is a metabolic intermediate of the de novo purine synthesis pathway presenting highly promising metabolic and antiproliferative properties. Yeast mutants accumulating AICAR are auxotroph for histidine. A screening for suppressors of this phenotype identified recessive and dominant mutants that result in lowering intracellular AICAR concentration. The recessive mutants affect adenosine kinase which is shown here to catalyze the phosphorylation of AICAR riboside in yeast. The dominant mutants strongly enhance the capacity of the alkaline phosphatase Pho13p to dephosphorylate succinyl-AICAR monophosphate into the non-toxic riboside form. By combining these mutants to transcriptomic and metabolomic analyses, we establish that in yeast both toxic and physiological responses to AICAR are linked to the concentration of the monophosphate form, while the nucleoside moiety has no effect even at high concentration. Finally, we establish that (S)AICAR concentration varies under physiological conditions, thus modulating transcriptional regulation of purine pathway genes. This SuperSeries is composed of the SubSeries listed below.
2011-07-11 | GSE29324 | GEO
Project description:We have demonstrated AICAR can maintain J1 mouse ES cells pluripotency in our previous research, yet its effects on ES cells miRNAs expression remain a mystery. In this study, we performed small RNA (sRNA) High-throughput sequencing using Illumina HiSeq 2000 to investigate the influence of AICAR on J1 mouse ES cells miRNAs expression and further found the mechanism of how miRNAs affect ES cells pluripotency maintenance. Samples that treated by DMSO is used as a control. Compare microRNA expression of J1 mESC cultured with or without small molecule AICAR
2014-02-06 | E-GEOD-54586 | biostudies-arrayexpress
Project description:We have demonstrated AICAR can maintain J1 mouse ES cells pluripotency in our previous research, yet its effects on ES cells miRNAs expression remain a mystery. In this study, we performed small RNA (sRNA) High-throughput sequencing using Illumina HiSeq 2000 to investigate the influence of AICAR on J1 mouse ES cells miRNAs expression and further found the mechanism of how miRNAs affect ES cells pluripotency maintenance. Samples that treated by DMSO is used as a control.
2014-02-06 | GSE54586 | GEO
Project description:It has been demonstrated that CHIR99021 promotes self-renewal of mouse embryonic stem cells, however, the target genes of CHIR99021 is not fully understood. AICAR is the activator of AMP-activated protein kinase. It is reported that AICAR plays important role in mouse embryonic stem cells, however the moleculor mechanism of this phenomenon is unknown. To better understand the downstream target genes of CHIR99021 and AICAR, we performed Microarray analyses to identify their downstream targets. The data show the genes regulated by CHIR99021 or AICAR.
2013-01-01 | GSE40959 | GEO
Project description:It has been demonstrated that CHIR99021 promotes self-renewal of mouse embryonic stem cells, however, the target genes of CHIR99021 is not fully understood. AICAR is the activator of AMP-activated protein kinase. It is reported that AICAR plays important role in mouse embryonic stem cells, however the moleculor mechanism of this phenomenon is unknown. To better understand the downstream target genes of CHIR99021 and AICAR, we performed Microarray analyses to identify their downstream targets. The data show the genes regulated by CHIR99021 or AICAR. J1 mESCs maintained in medium containing 1000 U/mL LIF and supplemented without or with CHIR99021 or AICAR for 24 hours, then total RNA was extracted for analysis.
2013-01-01 | E-GEOD-40959 | biostudies-arrayexpress
Project description:The purpose of the research is to delineate the mechanism behind AICAR-induced cytotoxicity by understanding the genetic pathways that are affected with AICAR treatment.
2023-02-21 | GSE198777 | GEO
Project description:Skeletal muscle is a major contributor to whole-body glucose homeostasis and is an important endocrine organ. To date, few studies have undertaken the large-scale identification of skeletal muscle-derived secreted proteins (myokines), particularly in response to stimuli that activate pathways governing energy metabolism in health and disease. Whereas the AMP-activated protein kinase (AMPK) and insulin-signaling pathways have received notable attention for their ability to independently regulate skeletal muscle substrate metabolism, little work has examined their ability to re-pattern the secretome. The present study coupled the use of high-resolution MS-based proteomics and bioinformatics analysis of conditioned media derived from 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR – an AMPK activator)- and insulin-treated differentiated C2C12 myotubes. We quantified 858 secreted proteins, including cytokines and growth factors such as fibroblast growth factor-21 (Fgf21). We identified 377 and 118 proteins that were significantly altered by Insulin and AICAR treatment, respectively. Notably, the family of insulin growth factor binding-proteins (Igfbp) was differentially regulated by each treatment. Insulin- but not AICAR-induced conditioned media increased the mitochondrial respiratory capacity of myotubes, potentially via secreted factors. These findings may serve as an important resource to elucidate secondary metabolic effects of insulin and AICAR stimulation in skeletal muscle.
2021-09-15 | PXD025687 | Pride
Project description:Transcription of immediate early genes (IEGs) in neurons is exquisitely sensitive to neuronal activity, but the mechanism underlying the earliest of these transcription events is largely unknown. Here we demonstrate that very fast IEGs (VF-IEGs) such as arc/arg3.1 are poised for rapid transcription by the stalling of RNA Polymerase II (Pol II) just downstream of the transcription start site. RNAi-depletion of two subunits of a mediator of Pol II stalling, Negative Elongation Factor, reduces Pol II occupancy of the arc promoter and compromises rapid induction of arc and other VF-IEGs. In contrast, reduction of Pol II stalling did not prevent expression of other fast IEGs (F-IEGs). These F-IEGs are expressed with comparatively slower kinetics and largely lack promoter proximal Pol II stalling. Taken together, our data strongly indicate that very fast kinetics of neuronal IEG expression require poised Pol II and suggest a role for this mechanism in transcription-dependent learning and memory. TTX withdrawal induced neuronal activity. To study activity-induced gene expression, neurons were treated with TTX for 48 hours and then TTX was washed out either for 15 minutes (W15) or for 45 minutes (W45). Gene expression was measured in these two groups in comparison to TTX treated neurons.
2011-04-14 | E-GEOD-22622 | biostudies-arrayexpress
Project description:U937 cells were treated wth 0.2 mM AICAr for 24 h to compare the results on cell line know to differentiate in the presence of AICAr with the results on primary patient sample.
2020-11-15 | E-MTAB-9537 | biostudies-arrayexpress