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Transcriptomic profile in in vitro produced mouse late two-cell stage embryos treated with MYC inhibitor 10074-G5

ABSTRACT: Transcriptomic profile in in vitro produced mouse late two-cell stage embryos treated with MYC inhibitor 10074-G5

PROVIDER: PRJNA978534 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24793414_1.fastq.gz	Fastqsanger.gz
	SRR24793414_2.fastq.gz	Fastqsanger.gz
	SRR24793415_1.fastq.gz	Fastqsanger.gz
	SRR24793415_2.fastq.gz	Fastqsanger.gz
	SRR24793416_1.fastq.gz	Fastqsanger.gz

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Transcriptomic profile in in vitro produced mouse late two-cell stage embryos treated with MYC inhibitor 10074-G5

Project description:Transcriptomic profile in in vitro produced mouse late two-cell stage embryos treated with MYC inhibitor 10074-G5

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Expression data from G0 versus G4/G5 CMP/GMP

Project description:Telomere dysfunctional CMP/GMP have deregulated pathways that are associated with DNA damage signaling We compared differentially expressed genes in the G4/G5 CMP relative to the G0 control to identify pathways that may affect CMP differentiation. Bone marrow CMP and GMP cells were sorted from two paired pools of G0 TERTER/+ or G4/G5 TERTER/ER mice (5,000-20,000 cells per sample) using the Influx Cell Sorter. Every paired pool includes CMP or GMP sorted from 4 age and gender matched G0 or G4/G5 mice. RNA from the respective sorted cells was extracted using Trizol (Ambion) and profiled on 2100 Bioanalyzer (Agilent). Gene expression profiling was performed at the Sequencing and Non-coding RNA Program at MD Anderson Cancer Center. Briefly, the GeneChip® 3 IVT Express Kit (Affymetrix) was used to generate biotin-labeled cRNA, which were purified and fragmented, before target hybridization on the GeneChip® Mouse Genome 430 2.0 Array (Affymetrix) according to the manufacturer's instructions. Affymetrix raw data (CEL files) were normalized using Affymetrix Microarray Suite (MAS) version 5.0 using a TGT=100. Paired pools used in the study were: CMP pool 1: G0-1 and G4/5-1 CMP pool 2: G0-2 and G4/G5-2 GMP pool 1: G0-1 and G4/G5-1 GMP pool 2: G0-2 and G4/G5-2

2015-04-09 | E-GEOD-62278 | biostudies-arrayexpress

A caspase-independent necrotic death is activated by isopeptidase inhibitor G5 in apoptosis-resistant glioblastoma cells

Project description:The regulation of necrotic death and its relevance in anti-cancer therapy are largely unknown. Here we have investigated the pro-apoptotic and pro-necrotic activities of two ubiquitin-proteasome system inhibitors (UPSIs): bortezomib and G5. The present study points out that the glioblastoma cell lines U87MG and T98G are useful models to study the susceptibility to apoptosis and necrosis in response to UPSIs. U87MG cells are resistant to apoptosis induced by bortezomib and G5 but susceptible to necrosis induced by G5. On the opposite T98G cells are susceptible to apoptosis induced by both inhibitors but show some resistance to G5-induced necrosis. By comparing the transcriptional profiles of the two cell lines, we have found that the resistance to G5-induced necrosis could arise from differences in glutathione synthesis/utilization and in the microenvironment. In particular collagen IV, which is highly expressed in T98G cells, and fibronectin, whose adhesive function is counteracted by tenascin-C in U87MG cells, can restrain the necrotic response to G5. Collectively, our results provide an initial characterization of the molecular signals governing cell death by necrosis in glioblastoma cell lines. Keywords: cell line comparison

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Expression data from G0 versus G4/G5 CMP/GMP

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Reduced representation bisulfite sequencing from G0 & G4/G5 CMP

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Umbilical cord blood methylome analysis of IVF neonates that underwent embryo culture in G5 or HTF medium

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Mettl3 regulates late-stage retinogenesis

Project description:Mettl3 regulates late-stage retinogenesis

| PRJNA749618 | ENA

Pisolithus microcarpus strain:G5

Project description:Pisolithus microcarpus G5 Resequencing

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Characterization of late-stage Drosophila grainy head IM-allele (grhIM) mutant embryos

Project description:To determine the genes directly and indirectly under the control of the Grainy head transcription factor during late stages of Drosophila embryogenesis.

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Reduced representation bisulfite sequencing from G0 & G4/G5 CMP

Project description:Differential hyper- and hypo-methylation regions in G0 versus G4/G5 CMP The goal of this study is to evaluate changes in CpG methylation profilings of telomere dysfunctional common myeloid progenitor cells (CMP) as compared to their wild type controls Genomic DNA was extracted from sorted CMP populations isolated from 3 pools of G0 or 2 pools of G5 mice using UltraPure Phenol:Chloroform:Isoamyl Alcohol according to manufacturer’s instructions (Life Technologies). 14,000 to 30,000 cells were available for each sample, resulting in a minimum of 45ng of DNA. Genome-wide DNA methylation profiling was performed by RRBS. Library preparation and sequencing were performed at the UT MD Anderson Cancer Center’s DNA Methylation Analysis Core and Sequencing and Microarray Facility, according to published protocols. RRBS sequencing data were aligned and methylation was called using Bismark v0.7.119. In brief, bisulphite-treated DNA was aligned to UCSC Genome Browser mm10 reference genome using Bowtie. In total 29-38 million reads were generated per sample with alignment rates around 63%. Next, MethylKit10 implemented with Fisher’s exact test was used to compare the cytosine methylation profiles of G0 and G5 CMP. Gene promoter regions were calculated based on RefSeq gene annotations with regions starting 1 kb upstream of the annotated transcription start site (TSS) and extending 500 base pairs downstream of TSS. Exons, introns, and CpG islands coordinates were collected from the UCSC Genome Browser mm10 version.

2015-04-09 | E-GEOD-62392 | biostudies-arrayexpress

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