Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10074600.fastq.gz | Fastqsanger.gz | |||
| SRR10074700.fastq.gz | Fastqsanger.gz | |||
| SRR10074601.fastq.gz | Fastqsanger.gz | |||
| SRR10074701.fastq.gz | Fastqsanger.gz | |||
| SRR10074602.fastq.gz | Fastqsanger.gz |
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Project description:T and CAR T cells were generated from mock or CD19CAR+ Tn/mem-derived induced pluripotent stem cells (Tn/mem-iPS) by 3D-organoid culture system. We performed RNA deep sequencing analysis to better elucidate their phenotype and compare their gene expression profiles among groups of Tn/mem-iPSC derived T/ CAR T cells, PBMC derived T/CAR T cells, PBMC derived NK cells and T-iPSC cells, as well as CD4 and CD8 subsets of iPSC derived or PBMC derived CAR T cells.
2022-02-01 | GSE193422 | GEO
Project description:To assess the effect of different forms of TL1A within different organs of the mouse we generated 2 different transgenic mouse lines where TL1A was expressed under the control of the CD2 promoter. 2 forms of TL1A was used. Either WT TL1A, which led to over expression of both membrane bound and soluble forms of TL1A (Refered to as Mem+Sol) or TL1A Delta 69-93 which only overexpressed membrane restricted TL1A (Refered to as Mem). Lungs and terminal ileums were taken from Either Mem, Mem+sol or WT litermate control mice at 12 weeks of age and the transcriptome assessed using RNAseq Through this we demonstrated enrichment of different transcripts and pathways both dependent on and independent of the form of TL1A and the site of action. This study is also the first to use RNASeq to assess the resualt of overexpression of TL1A within the mouse.
2017-12-14 | GSE98492 | GEO
Project description:We investigated how varying the composition of cell culture formulations and growing cancer cells at different densities might affect tumor cells genotype. Specifically, we compared gene expression profiles generated by human MDA-MB-231 human breast cancer cells cultured in different media (MEM, DMEM, or RPMI 1640) containing different concentrations of fetal bovine serum (FBS) or different sera (equine or bovine) that were grown at different cell densities. We have 6 different group (1. MDA-MB-231; MEM-10% FBS-90% confluence (MEM-1 and MEM-2). 2. MDA-MB-231; DMEM-10% FBS-90% confluence (DMEM-1 and DMEM-2). 3. MDA-MB-231; RPMI1640-10% FBS-90% confluence (RPMI-1 and RPMI-2) 4. MDA-MB-231; MEM-10% Horse serum-90% confluence (Horse-1 and Horse-2). 5. MDA-MB-231; MEM-0.1% FBS-90% confluence (FBS0.1-1 and FBS0.1-2). 6. MDA-MB-231; MEM-10% FBS-50% confluence (Con50-1 and Con50-2). Each group has duplicated. We analyzed; 1. Cell density (90% vs 50% confluence). 2. FBS concentration (10% FBS vs 0.1% FBS). 3. Sera (10% FBS vs 10% Horse serum). 4. Media (MEM vs DMEM vs RPMI1640)
2015-06-17 | E-GEOD-61670 | biostudies-arrayexpress
Project description:Escherichia coli MEM genome sequencing and assembly
| PRJNA292040 | ENA
Project description:Tet-mediated DNA oxidation is a new type of epigenetic modification in mammals and its role in the regulation of cell fate transition remains poorly understood. Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three Tet genes and examine their capability to be reprogrammed into iPS cells. We demonstrate that these Tet-deficient MEFs cannot be reprogrammed due to a blockage in the mesenchymal-to-epithelial transition (MET). Reprogramming of MEFs deficient in TDG is similarly blocked. The blockage is caused by impaired activation of crucial microRNAs, which depends on oxidative demethylation promoted by Tet and TDG. Reintroduction of either miR-200c or catalytically active Tet and TDG restores reprogramming to the respective knockout MEFs. Thus, oxidative demethylation is essential for somatic cell reprogramming. These findings provide mechanistic insights into the operation of epigenetic barriers in cell lineage conversion. Reduced Representation Bisulfite (RRBS, MspI,~75-400bp size fraction) and Tet-Assisted RRBS (TARRBS) of MEFs & reprogramming MEFs at Day 5
2014-02-19 | E-GEOD-52741 | biostudies-arrayexpress
Project description:The Ten-eleven translocation (TET) family of dioxygenases can mediate cytosine demethylation by catalyzing the oxidation of 5-methylcytosine (5mC). TET-mediated DNA demethylation controls the proper differentiation of embryonic stem cells and TET proteins display functional redundancy during early gastrulation. However, it is unclear if TET proteins have functional significance in mammalian skeletal development. Here, we report that Tet deficiency in mesoderm mesenchymal stem cells results in severe defects of bone development. The existence of any single Tet gene allele can support early bone formation, suggesting a potential functional redundancy of TET proteins. Integrative analyses of RNA-seq, Whole Genome Bisulfite Sequencing (WGBS) and Assay for Transposase-Accessible Chromatin (ATAC-seq) demonstrate that TET-mediated demethylation increases the chromatin accessibility of target genes by RUNX2 and facilities RUNX2-regulated transcription. In addition, TET proteins interact with RUNX2 through their catalytic domain to regulate cytosine methylation around RUNX2 binding region. The catalytic domain is indispensable for TET proteins to regulate RUNX2 transcription activity on its target genes and to regulate bone development. These results demonstrate that TET proteins function redundantly to regulate RUNX2 activity via dual mechanisms and maintain skeletal homeostasis.
2022-07-07 | GSE174045 | GEO
Project description:Transcriptional profiling of Campylobacter jejuni NCTC 11168 wild type versus LuxS01 mutant strain grown in a minimal culture medium (MEM- α ) versus complex culture medium (MHB).
2009-10-08 | GSE18451 | GEO
Project description:Mammalian genomes are subjected to epigenetic modifications, including cytosine methylation by DNA methyltransferases (Dnmt) and further oxidation by Ten-eleven-translocation (Tet) family of dioxygenases. Cytosine methylation plays key roles in multiple processes such as genomic imprinting and X-chromosome inactivation. However, the functional significance of cytosine methylation and the further oxidation has remained undetermined in mouse embryogenesis. Here we show that global inactivation of all three Tet genes in mice led to consistent defects in gastrulation. The defects include reduced specification of the axial mesoderm and paraxial mesoderm, mimicking phenotypes in embryos with gain-of-function Nodal signaling, a cardinal cue for gastrulation. Introduction of a single mutant allele of Nodal in the Tet mutant background partially restored patterning, suggesting that hyperactive Nodal signaling is a leading cause for the gastrulation failure of Tet mutants. Increased Nodal signaling is likely due to diminished expression of the Lefty1 and Lefty2 genes, inhibitors of Nodal signaling. Moreover, reduction in the Lefty gene expression can be ascribed to elevated DNA methylation as both Lefty-Nodal signaling and normal morphogenesis are largely restored in Tet-deficient embryos when the Dnmt3a and Dnmt3b genes are disrupted. Additionally, specific inactivation of Tet by point mutations abolishing the dioxygenase activity causes similar molecular and gastrulation abnormalities. Taken together, our results show that Tet-mediated DNA oxidation modulates the Lefty-Nodal signaling by promoting demethylation of the shared target genes with Dnmt3a and Dnmt3b. These findings reveal a fundamental epigenetic mechanism featuring dynamic DNA methylation and demethylation and their role in the regulation of key signaling in body plan formation during early embryogenesis. Examine RNA expression and DNA methylation differences between Tet-null and wild type samples of mouse epiblast in E6.5.
2016-10-27 | E-GEOD-76261 | biostudies-arrayexpress
Project description:Modifications of mRNA, especially methylation of adenosine, have recently drawn much attention. The much rarer modification, 5-hydroxymethylation of cytosine (5hmC), is not well understood and is the subject of this study. Vertebrate Tet proteins are 5-methylcytosine (5mC) hydroxylases enzymes catalyzing the transition of 5mC to 5hmC in DNA and have recently been shown to have the same function in messenger RNAs in both vertebrates and in Drosophila. The Tet gene is essential in Drosophila because Tet knock-out animals do not reach adulthood. We describe the identification of Tet-target genes in the embryo and larval brain by determining Tet DNA-binding sites throughout the genome and by mapping the Tet-dependent 5hmrC modifications transcriptome-wide. 5hmrC-modified sites can be found along the entire transcript and are preferentially located at the promoter where they overlap with histone H3K4me3 peaks. The identified mRNAs are frequently involved in neuron and axon development and Tet knock-out led to a reduction of 5hmrC marks on specific mRNAs. Among the Tet-target genes were the robo2 receptor and its slit ligand that function in axon guidance in Drosophila and in vertebrates. Tet knock-out embryos show overlapping phenotypes with robo2 and are sensitized to reduced levels of slit. Both Robo2 and Slit protein levels were markedly reduced in Tet KO larval brains. Our results establish a role for Tet-dependent 5hmrC in facilitating the translation of modified mRNAs, primarily in developing nerve cells.
2024-02-23 | GSE225970 | GEO