Genome-wide analysis of gene expression regulated by nucleolin in mouse embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Ying Jin
PROVIDER: E-GEOD-23993 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To further explore the function and underlying mechanism of nucleolin in embryonic stem cells (ESCs), we compared the transcription profile of tetracycline (Tc)-inducible EGFP (as a control) or nucleolin siRNA expression-stable ESCs cultured with or without Tc for 3 days, and identified distinct classes of up- and down-regulated genes by nucleolin in mouse ESCs.
2011-10-20 | GSE23993 | GEO
Project description:Self-renewal and pluripotency are hallmarks of embryonic stem cells (ESCs). However, signaling pathways triggering their transition from self-renewal to differentiation are not well defined. Here, we report that the calcineurin-NFAT signaling pathway is both necessary and sufficient to switch ESCs from an undifferentiated state to early differentiation.To gain an insight into the function of calcinerin-NFAT signaling in ESC lineage commitment, we examined the repertoire of genes changed after LIF withdrawal alone, LIF withdrawal in the presence of cyclosporine A (CsA), a specific inhibitor of calcinerin and forced expression of active forms of calcineurin (deltaCnA) in the presence of LIF,and identified distinct classes of up and down regulated genes by calcineurin-NFAT signaling in mouse embryonic stem cells. Total RNA obtained from CGR8 ES cells under the following conditions: withdrawal of LIF for 0, 1 and 3 days; withdrawal of LIF for 0, 1 and 3 days in the presence of CsA, and induced expression of deltaCnA by withdrawal of Tc for 0, 1 and 4 days in ideltaCnAES cells.Hybridized to Illumina Sentrix Mouse-6 v1.1 Beadhips
2011-01-01 | E-GEOD-21378 | biostudies-arrayexpress
Project description:To study if the transcriptional content in exosomes derived from unntreated and growth factor treated cultured cardiomyocytes (HL-1) differ and if so, can this difference be explained.This is results for the cells.The exosome reults can be find at GSE40503. 4 control untreated samples, 4 TFG-beta2 cardiomyocyte treated samples and 4 PDGF BB cardiomyocyte were studied., this reults are from the corresponding cells (that released the exosomes), used for data filtering of the exsomedata. The exosome reults can be find at GSE40503.
2013-06-20 | E-GEOD-45207 | biostudies-arrayexpress
Project description:Mammary gland (MG) de novo lipogenesis contributes significantly to milk fat in animals but little is known in humans. We hypothesized that de novo lipogenesis, as reflected by incorporation of 13C carbons from [U-13C]glucose into fatty acids (FAs) and glycerol in triglycerides (TG), will be greater: a. in milk than plasma TG, b. during a high carbohydrate (H-CHO) diet than high fat (H-FAT) diet and c. during feeding than fasting. Healthy lactating women were studied on two isocaloric, isonitrogenous diets. On one occasion subjects received diets containing H-FAT or H-CHO diet for 1 week. Incorporation of 13C from infused [U-13C]glucose into FAs and glycerol was measured using GC/MS methodology and gene expression using RNA isolated from breast milk fat globule (MFG). Incorporation of 13C2 into milk FAs, increased with increased chain length of the FAs from C2:0 to C12:0 but progressively declined in C14:0 and C16:0 and was not detected in FAs >C16. During feeding, regardless of diets, enrichment of 13C2 in milk FA and 13C3 in milk glycerol were ~3 and ~7 fold higher compared to plasma FA and glycerol, respectively. Following an overnight fast during H-CHO and H-FAT diets study periods, 25% and 6%, respectively, of medium chain FAs (MCFAs, C6-C12) were derived from glucose but increased to 75% and 25% with feeding. The expression of genes involved in FA or glycerol synthesis pathways was unchanged regardless of diet or fast-fed conditions. Conclusions: The human MG is capable of de novo lipogenesis, of primarily MCFAs and glycerol, which is influenced by the macro-nutrient composition of the maternal diet. On day 7 of consumption of each of the two diets milk samples collected from 7 healthy, lean, exclusively breastfeeding women following an overnight fast and feeding conditions [7 x 2 x 2 = 28 samples] were processed for isotope enrichments and RNA isolation from the milk fat globules. The total RNA was utilized for microarray analyses.
2014-05-19 | E-GEOD-51874 | biostudies-arrayexpress
Project description:Profiling global gene expression of undifferentiated human embryonic stem cells, artificially derived cardiomyocytes, fetal ventricular cardiomyocytes, and adult ventricular cardiomyocytes to determine transcriptomic variation between these cell types. Total RNA extracted from 10 human samples representing four stages of cardiac development from undifferentiated stem cells to mature adult cardiac tissue.
2013-09-10 | E-GEOD-50704 | biostudies-arrayexpress
Project description:Various substances have been reported to enhance the cardiac differentiation of embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). Ascorbic Acid had a cardiogenic effect in mESC CGR8 cell line. Transcriptome of AA-treated CGR8 ESCs did not reveal any significant changes in gene expression as compared to untreated cells. We performed a global gene expression analysis to better understand the mechanism of Ascorbic acid-induced cardiac differentiation.
2015-05-21 | GSE54242 | GEO
Project description:One of most common events in carcinogenesis is loss of DNA methylation (hypomethylation) from sequence of transposable element (TEs) including long interspersed nuclear element-1 (LINE-1). Naturally, LINE-1 and other TEs within gene body region (intragenic) will suppress by fully methylated CpG sequences in order to keep prevent incorrect transcriptional start site (TSSs) that cause genome instability. To study character of intragenic LINE-1 promoter hypomethylation or gene body methylation status, within Head and Neck squamous cell carcinoma (HNSCC) cell, LINE-1 promoter methylation status was detected with CU-L1 (unique intragenic LINE-1) and COBRALINE-1 (whole genome LINE- 1) PCRs. Each intragenic LINE-1 promoter hypomethylation have unique pattern depending on cell types and impact of LINE-1M-bM-^@M-^Ys host gene within cell. From CU-L1 PCR 16 genes, EPHA3 and PPP2R2B are only two genes that normally induce expression by hypermethylated in gene body region, intragenic LINE-1 promoter. LINE-1 promoter hypomethylation level induce global and specific LINE-1 expression and also repress LINE-1M-bM-^@M-^Ys host genes expression, which confirm by 5M-bM-^@M-^Y- aza-2-deoxycytidine induced DNA hypomethylationin HNSCC cell that cause EPHA3 become greater down- regulated. Since LINE-1 RNA can express via promoter hypomethylation, knockdown LINE-1 RNA can lead increasing of EPHA3 in HNSCC cell. LINE-1 RNA was concern as key factor on LINE-1 hostM-bM-^@M-^Ys gene regulation by consequence of gene body hypomethylation. RNA molecule can regulate gene by RNAi pathway and Epigenetics mechanism, within both machinery require RISC proteins. Next, knockdown RISC protein, DICER1 gene can investigate possibility role that LINE-1 RNA regulate LINE-1 host gene. Within yeast cell, overexpress retrotransposon transcript was control by endo-siRNA pathway, which require DICER1 like protein for produce endo-siRNA from precursor molecule that include retrotransposon transcript. With CU-DREAM analyse microarray results by intersection datas for check the connection between factors on gene regulation including DICER1, LINE-1 RNA, DNA hypomethylation and HNSCC carcinogenesis model. According to CU-DREAM analysis for HNSCC cell panel, DICER1 involved pathway may induce hypermethylation on gene body region which relate to TSS and intragenic LINE-1 promoter region. While LINE-1 RNA involved pathway select to induce hypermethylation on gene without LINE-1 promoter, LINE-1 RNA have in tran function. In conclusion, intragenic LINE-1 promoter hypomethylation cause releases of LINE-1 RNA for regulate genes during HNSCC carcinogenesis via RISC protein. Oligonucleotides specific target on LINE-1 was inserted into Psilencer 3.1 vector hygro H1 promoter. (Ambion, Austin, Texas, USA) and transfection was mediated by FuGENE M-BM-. HD (Roche), sequence shown in appendix. Oligosynthesis siRNA specific to DICER1 purchased from santa cruz biotechnology for transient tranfection, inc was dilute with RNASE free dH2O to reach 10M-NM-<M. In a 12 well plate, seed 6 x 105 cells per well in 1 ml antibiotic-free normal growth medium supplemented with 10% FBS. In next day, perform transfection those siRNA at 100 nM with Lipofectamine 2000 reagent (Invitrogen Cat: 11668-027) according to the manufacturer's instructions. Cell was collect at 48h after transfection step by Trizol reagent (Life technologies, Inc.) in order to collect total RNA from each sample for hybridize on beadchip according to the protocol.
2012-11-05 | E-GEOD-33493 | biostudies-arrayexpress
Project description:One third of BRAF-mutant metastatic melanoma patients treated with combined BRAF and MEK inhibition progress within six months. Treatment options for these patients remain limited. Here we analyse twenty BRAFV600 mutant melanoma metastases derived from 10 patients treated with the combination of debrafenib and trametinib for resistance mechanisms and genetic correlates of response. Resistance mechanisms are identified in 9/11 progressing tumors and MAPK reactivation occurred in 9/10 tumors, commonly via BRAF amplification and mutations activating NRAS and MEK2. Our data confirming that MEK2C125S, but not the synonymous MEK1C121S protein confers resistance to combination therapy, highlight the functional differences between these kinases and the preponderance of MEK2 mutations in combination therapy-resistant melanomas. Exome sequencing did not identify additional progression-specific resistance candidates. Nevertheless, most melanomas carried additional oncogenic mutations at baseline (e.g. RCA1 and AKT3) that activate the MAPK and P13K pathways and are thus predicted to diminish response to MAPK inhibitors. Total RNA obtained from fresh frozen melanoma tumors treated with a combination of dabrafenib and trametinib
2014-12-03 | E-GEOD-61992 | biostudies-arrayexpress
Project description:Inhibitors of the MAPKs, BRAF and MEK, induce tumor regression in the majority of patients with BRAF-mutant metastatic melanoma. The clinical benefit of MAPK inhibitors is restricted by the development of acquired resistance with half of those who benefit having progressed by 6-7 months and long-term responders uncommon. There remains no agreed treatment strategy on disease progression in these patients. Without published evidence, fears of accelerated disease progression on inhibitor withdrawal have led to the continuation of drugs beyond formal disease progression. We now demonstrate that treatment with MAPK inhibitors beyond disease progression can provide significant clinical benefit, and the withdrawal of these inhibitors led to a marked increase in the rate of disease progression in two patients. We also show that MAPK inhibitors retain partial activity in acquired resistant melanoma by examining drug-resistant clones generated to dabrafenib, trametinib or the combination of these drugs. All resistant sublines displayed a markedly slower rate of proliferation when exposed to MAPK inhibitors, and this coincided with a reduction in MAPK signalling, decrease in BrdU incorporation and S-phase inhibition. This cytostatic effect was also associated diminished levels of cyclin D1 and p-pRb.. Two short-term melanoma cultures generated from resistant tumour biopsies also responded to MAPK inhibition with comparable inhibitory changes in proliferation and MAPK signalling. These data provide a rationale for the continuation of BRAF and MEK inhibitors after disease progression and support the development of clinical trials to examine this strategy. Total RNA obtained from melanooma cell lines treated for 24h with dabrafenib, trametinib or combination of dabrafenib and trametinib
2013-06-30 | E-GEOD-44753 | biostudies-arrayexpress
Project description:We show that mice lacking Siglec-E, the main member of the CD33rSiglec family, exhibit reduced survival. Removal of Siglec-E causes the development of exaggerated signs of aging at the molecular, structural, and cognitive level. We found that accelerated aging was related both to an unbalanced ROS metabolism, and to a secondary impairment in detoxification of reactive molecules, ultimately leading to increased damage to cellular DNA, proteins and lipids. Taken together, our data suggest that CD33rSiglecs co-evolved in mammals to achieve a better management of oxidative stress during inflammation, which in turn reduces molecular damage and extends lifespan. Total RNA obtained from liver tissues from two wild-type and three Siglec-E-deficient mice
2016-01-15 | E-GEOD-64760 | biostudies-arrayexpress