RNA-seq of U937 cells treated with AICAr
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 4000
ORGANISM(S): Homo sapiens
SUBMITTER: Vilma Dembitz
PROVIDER: E-MTAB-9537 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Ribonucleoside AICAr, a precursor in purine synthesis and a known activator of AMPK, was shown to induce monocytic differentiation in AML cell lines by inducing pyrimidine depletion followed by activation of ATR/Chk1 pathway and cell cycle arrest. Here we report transcriptional changes induced by AICAr in the primary AML sample (FAB-M2, FLT3 negative, NPM1 negative) in which AICAr induced differentiation and accumulation of macrophage cells in vitro. RNA-seq transcriptome analysis of primary AML cells isolated from the bone marrow of a patient with de novo FAB-M2 AML. Mononuclear cells were isolated from the bone marrow sample by density gradient separation and grown in RPMI supplemented with 10% FBS, 2 mM L-glutamine, 50 U/ml penicillin, 50 μg/ml streptomycin and 50 ng/ml IL-3, IL-6, SCF and FLT3L. Cells were treated with AICAr (0.4 mM) for 24 h. Experiment was performed in biological triplicates and total RNA was isolated for transcriptome analysis using Illumina high throughput sequencing.
2020-11-01 | E-MTAB-9209 | biostudies-arrayexpress
Project description:We investigated the role of Ado1p associated with AICAr supplementation on the global transcriptome of Y3188. The Y3188 strain was grown with or without AICAr. For each comparison, we made 2 biological replicates, swapping dyes.
2011-08-31 | E-GEOD-29020 | biostudies-arrayexpress
Project description:We investigated the effects of AICAr supplementation on the global transcriptome of Y2950. The Y2950 strain was grown with or without AICAr. For each comparison, we made 2 biological replicates, swapping dyes.
2011-08-31 | E-GEOD-29019 | 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. Compare microRNA expression of J1 mESC cultured with or without small molecule AICAR
2014-02-06 | E-GEOD-54586 | biostudies-arrayexpress
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:Normal aging can result in a decline of memory and muscle function. Exercise may prevent or delay these changes. However, aging associated frailty may preclude physical activity. AMP-activated protein kinase (AMPK) is a transcriptional regulator important for muscle physiology. In the present study we investigated effects of AMPK agonist 5-aminoimidazole-4-carboxamide riboside (AICAR) on memory and motor function in young (2-month-old), aged (23-month-old) C57Bl/6 mice, and transgenic mice with muscle-specific mutated AMPK alpha-subunit (AMPK-DN). Mice were injected with AICAR (500 mg/kg) for 3 to 14 days and tested in the Morris water maze, rotarod and open field. Improved water maze performance and motor function was observed, albeit at longer duration of administration, in aged (14 days AICAR) than young (3 days AICAR) mice. In the AMPKDN mice, the compound did not enhance behavior, providing support for a muscle mediated mechanism. In addition, microarray analysis of muscle and hippocampal tissue derived from aged mice treated with AICAR revealed changes in gene expression in both tissues, which correlated with behavioral effects in a dose-dependent manner. Pronounced up-regulation of mitochondrial genes in muscle was observed. In the hippocampus genes relevant to neuronal development and plasticity were enriched. Altogether, endurance related factors may mediate both muscle and brain health in aging, and could play a role in new therapeutic interventions. Key words: Skeletal Muscle, Brain, Exercise, AMPK, Learning and Memory, Morris water maze 23-month old female C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME) were housed under standard conditions, 3 mice per cage, with food and water ad libitum. Mice were injected intraperitoneally with 5-Aminoimidazole-4-carboxamide-1-a-D-ribofuranoside (AICAR, Toronto Research Chemicals Inc., Canada) dissolved in saline, 500 mg/kg/day for 3 (ACR3), 7 (ACR7) or 14 (ACR14) days or saline vehicle, for 3 (CTR) days. Thirty-three days after the final injection animals were deeply anesthetized with isofluorane and perfused transcardially with 0.9% NaCl solution. The gastrocnemius muscle and Hippocampus were quickly removed, frozen on dry ice and stored at M-bM-^HM-^R80 M-BM-0C for RNA isolation and microarray analysis.
2014-01-17 | E-GEOD-50873 | biostudies-arrayexpress
Project description:Based on genetic and affinity chromatography experiments, the karyopherin Kap123 was identified as an important player in the cellular response to the drug acadesine (AICAR, 5′-phosphoribosyl-5-amino-4-imidazole carboxamide). Since Kap123 mediates nuclear import of multiple proteins we hypothesized that AICAR could affect nuclear trafficking. The effect of acadesine (AICAR) on nuclear trafficking was assayed by comparing protein composition of enriched nuclear extracts from yeast treated or not with AICAR by label-free quantitative analysis. Total protein extracts from the same cultures were also assayed by quantitative mass spectrometry. A parallel analysis was performed on yeast cells grown in the presence of AICAR and overexpressing or not Kap123 to identify those proteins that are enriched in the nuclear fraction when Kap123 was overexpressed.
2018-11-23 | PXD007779 | Pride
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:To candidate phosphorylation sites of ORP8 in cells and the stoichiometric change of ORP8's phosphorylation when AMPK is activated,LC-MS/MS analysis of ORP8 immunoprecipitated from serum-starved cells and cells treated with AMPK activator AICAR was performed.
2023-10-24 | PXD036204 | Pride
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