IlEucMixx1
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53874 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| CALYKY02.dat.gz | Other | |||
| CALYKY02.fasta.gz | Fasta.gz | |||
| CALYKY02.master.dat | Other |
Items per page: 5 1 - 4 of 4 |
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Project description:Euclidia mi (Mother Shipton) genome assembly, ilEucMixx1, alternate haplotype
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Project description:Genome wide DNA Methylation in fetal cord blood and placenta from mother with GDM compared to mother with normal glucose tolerance
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Project description:Genome wide DNA Methylation in fetal cord blood and placenta from mother with GDM compared to mother with normal glucose tolerance
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Project description:Purpose: Acupuncture exerts cardioprotective effects on several types of cardiac injuries, especially myocardial ischemia (MI). In order to elucidate the potential mechanisms, RNA-seq by next generation sequencing was used to identify the rat genome-wide alterations after MI and EA treatment in this study Methods: Adult male Sprague Dawley rats (250-300g) were divided into three groups: Control, MI and electro-acupuncture (EA) groups, myocardium mRNA profiles of rats in each group were generated by deep sequencing,using Illumina Hiseq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 25 million sequence reads per sample to the mouse genome (UCSC RN4) and identified 121,233, 178,242, 161,880 transcripts in the Control, MI and EA rats with TopHat and Cufflinks workflow respectively. Approximately 32% and 22% of the transcripts showed differential expression between the Control and MI, MI and EA respectively with a fold change â¥2.0. Conclusions: Our results for the first time generated genome-wide gene expression profiles both in the rat MI model and in acupuncture treatment by high throughput sequencing. The optimized data analysis workflows reported here should provide a framework for acupuncture investigations of expression profiles. Myocardium mRNA profiles of Control, MI and EA rats were generated by Hiseq 2000, Control and MI+EA group there were three samples, MI group there were two samples.
2016-03-21 | E-GEOD-54132 | biostudies-arrayexpress
Project description:Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single cell RNA-Seq, ChiP-Seq, concordant perturbations in ATAC-Seq and RNA-Seq peaks, RPPA and CyTOF analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1. MI-mediated genome-wide, concordant, log2 fold-perturbations (up or down-regulation) in ATAC-Seq and RNA-Seq peaks were observed at the loci of MLL-FP target genes, with upregulation of mRNAs associated with AML differentiation. scRNA-Seq analysis of bone marrow aspirate (BMA) cells harboring MLL1-FP and FLT3 mutation revealed enrichment of gene-sets of TNFα, interferon α/γ, inflammatory response and apoptosis gene-sets, but negative enrichment of the gene-set of MYC targets. Notably, MI treatment reduced the number of cells expressing the stem/progenitor cell signature. A protein domain-focused CRISPR-Cas9 screen in MLL1-r AML cells identified targetable co-dependencies with MI treatment, including BRD4, EP300, MOZ and KDM1A. Consistent with this, in vitro co-treatment with MI and BET, MOZ, LSD1 or CBP/p300 inhibitor induced synergistic loss of viability of AML cells with MLL1-r or mtNPM1. Co-treatment with MI and BET or CBP/p300 inhibitor also exerted significantly superior in vivo efficacy in xenograft models of AML with MLL1-r. These findings highlight novel, MI-based combinations that could prevent escape of AML stem/progenitor cells following MI monotherapy and could potentially prevent therapy-refractory relapse of AML with MLL1-r or mtNPM1.
2023-04-19 | GSE228323 | GEO
Project description:Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single cell RNA-Seq, ChiP-Seq, concordant perturbations in ATAC-Seq and RNA-Seq peaks, RPPA and CyTOF analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1. MI-mediated genome-wide, concordant, log2 fold-perturbations (up or down-regulation) in ATAC-Seq and RNA-Seq peaks were observed at the loci of MLL-FP target genes, with upregulation of mRNAs associated with AML differentiation. scRNA-Seq analysis of bone marrow aspirate (BMA) cells harboring MLL1-FP and FLT3 mutation revealed enrichment of gene-sets of TNFα, interferon α/γ, inflammatory response and apoptosis gene-sets, but negative enrichment of the gene-set of MYC targets. Notably, MI treatment reduced the number of cells expressing the stem/progenitor cell signature. A protein domain-focused CRISPR-Cas9 screen in MLL1-r AML cells identified targetable co-dependencies with MI treatment, including BRD4, EP300, MOZ and KDM1A. Consistent with this, in vitro co-treatment with MI and BET, MOZ, LSD1 or CBP/p300 inhibitor induced synergistic loss of viability of AML cells with MLL1-r or mtNPM1. Co-treatment with MI and BET or CBP/p300 inhibitor also exerted significantly superior in vivo efficacy in xenograft models of AML with MLL1-r. These findings highlight novel, MI-based combinations that could prevent escape of AML stem/progenitor cells following MI monotherapy and could potentially prevent therapy-refractory relapse of AML with MLL1-r or mtNPM1.
2023-04-19 | GSE228325 | GEO
Project description:Monotherapy with Menin inhibitor (MI), e.g., SNDX-5613, induces clinical remissions in patients with relapsed/refractory AML harboring MLL1-r or mtNPM1, but most patients either fail to respond or eventually relapse. Utilizing single cell RNA-Seq, ChiP-Seq, concordant perturbations in ATAC-Seq and RNA-Seq peaks, RPPA and CyTOF analyses, present pre-clinical studies elucidate gene-expression correlates of MI efficacy in AML cells harboring MLL1-r or mtNPM1. MI-mediated genome-wide, concordant, log2 fold-perturbations (up or down-regulation) in ATAC-Seq and RNA-Seq peaks were observed at the loci of MLL-FP target genes, with upregulation of mRNAs associated with AML differentiation. scRNA-Seq analysis of bone marrow aspirate (BMA) cells harboring MLL1-FP and FLT3 mutation revealed enrichment of gene-sets of TNFα, interferon α/γ, inflammatory response and apoptosis gene-sets, but negative enrichment of the gene-set of MYC targets. Notably, MI treatment reduced the number of cells expressing the stem/progenitor cell signature. A protein domain-focused CRISPR-Cas9 screen in MLL1-r AML cells identified targetable co-dependencies with MI treatment, including BRD4, EP300, MOZ and KDM1A. Consistent with this, in vitro co-treatment with MI and BET, MOZ, LSD1 or CBP/p300 inhibitor induced synergistic loss of viability of AML cells with MLL1-r or mtNPM1. Co-treatment with MI and BET or CBP/p300 inhibitor also exerted significantly superior in vivo efficacy in xenograft models of AML with MLL1-r. These findings highlight novel, MI-based combinations that could prevent escape of AML stem/progenitor cells following MI monotherapy and could potentially prevent therapy-refractory relapse of AML with MLL1-r or mtNPM1.
2023-04-19 | GSE228324 | GEO