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Mus musculus
18 Downloadable Samples
Illumina HiSeq 2500
Description
We have here followed the transcriptional effect of stimulation with the phorbol ester PMA in mouse fibroblasts from HP1gamma null mice recomplemented with either wild-type HP1gamma or an HP1g with an S83A mutation Overall design: Spontaneously immortalized mouse embryonic fibroblasts from HP1gamma null mice were used to stably integrate either an empty expression vector, or expression vectors for either WT or S83A mutant HP1gamma. These cells were then stimulated with PMA for 0 or 60 min. and used for transcriptome analysis by Next Generation sequencing.
Publication Title
Shigella flexneri targets the HP1γ subcode through the phosphothreonine lyase OspF.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 58 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Gene signatures were derived to separate responders from nonresponders by tipifarnib treatment.
Publication Title
Identification of molecular predictors of response in a study of tipifarnib treatment in relapsed and refractory acute myelogenous leukemia.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: The goals of this study are to elucidate dowstream effects of lnc RNA, Neat1 deletion in cerebral frontal cortex of adult mice by comparing Next-generation sequencing -derived cortical transcriptome profiles (RNA-seq) between wild type and Neat1 knockout mice. Methods: Brain mRNA profiles of 2-4 moths-old wild-type (WT) and lnc RNA, Neat1 knockout (Neat1-/-) mice were generated by deep sequencing, using Illumina. Reads were mapped to mm10 reference genome using TopHat (version 2.0.9) and Bowtie (version 2.1.0), with the default parameters. Known iGenomes Ensembl mm10 were quantified by HTSeq (version 0.6.0) in intersection-strict mode. A sample-by-gene read count matrix was generated for all samples by the Ensembl genes. Scaling normalization to remove composition biases in sequencing data was applied to log(CPM) (read Counts Per Million total reads) using the trimmed mean of M-values (TMM) method. Results: RNA-seq showed near-complete depletion of Neat1 RNA levels. 1359 genes were differentially expressed in the frontal cortex of Neat1-/- mice. 25 of these differentially expressed genes withstood multiple testing corrections. Examination of RNA-seq data by principle component analysis showed two principle components that were mutually uncorrelated and orthogonal. Hierarchical cluster tree analysis showed that joined nodes from Neat1-/- samples were distanced from control subset cluster confirming the results of the PCA. Conclusions: Analyses of differentially expressed gene signature from NEAT1-/- mice revealed a significant impact on processes related to oligodendrocyte differentiation and RNA post-transcriptional modification with the underlying mechanisms involving Wnt signaling, cell contact interactions, and regulation of cholesterol/lipid metabolism. Overall design: Cerebral frontal cortex mRNA profiles of 2-4 months old wild type (WT) and Neat1 -/- mice (all females) were generated by deep sequencing (N=5 controls; N=4 Neat1 knockout).
Publication Title
The expression of long noncoding RNA NEAT1 is reduced in schizophrenia and modulates oligodendrocytes transcription.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Subject
View Samples
SRP034832- Homo sapiens
- 30 Downloadable Samples
- IlluminaHiSeq2500
Description
IMR-32 cells were subjected to lentiviral YRNA infection or nELAVL RNAi and/or UV stress followed by RNAseq analysis to monitor RNA level changes Overall design: RNA from IMR-32 cells was Trizol extracted, Ribominus selected and submitted for high-throughput sequencing.
Publication Title
Regulatory consequences of neuronal ELAV-like protein binding to coding and non-coding RNAs in human brain.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 19 Downloadable Samples
- Illumina HiSeq 2500
Description
Early innate lymphoid progenitors (EILP) have recently been identified in the mouse adult bone marrow as a multipotential progenitor population committed to ILC lineages, but their relationship with other described ILC progenitors is still unclear. In this study, we examine the progenitor-successor relationships between EILP, IL-7R+ common lymphoid progenitors (ALP), and ILC precursors (ILCp). Bioinformatic, phenotypical, functional, and genetic approaches collectively establish EILP as an intermediate progenitor between ALP and ILCp. Our work additionally provides new candidate regulators of ILC development and clearly defines the stage of requirement of transcription factors key for early ILC development. Overall design: transcriptional profiling of early ILC progenitors (EILP, ILCp), and common lymphoid progenitors (ALP) was performed by RNA sequencing
Publication Title
Development and differentiation of early innate lymphoid progenitors.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 34 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Layer II stellate neurons (entorhinal cortex) and layer III cortical neurons (hippocampus CA1, middle temporal gyrus, posterior cingulate, superior frontal gyrus, primary visual cortex) were gene expression profiled. Brain regions are from non-demented individuals with intermediate Alzheimer's disease neuropathologies
Publication Title
Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
Description
Smyd3 is a histone methyltransferase implicated in tumorigenesis. Here we show that Smyd3 expression in mice is required but not sufficient for chemically induced liver and colon cancer formation. In these organs Smyd3 is functioning in the nucleus as a direct transcriptional activator of several key genes involved in cell proliferation, epithelial-mesenchymal transition, JAK/Stat3 oncogenic pathways, as well as of the c-myc and b-catenin oncogenes. Smyd3 specifically interacts with H3K4Me3-modified histone tails and is recruited to the core promoter regions of many but not all active genes. Smyd3 binding density on target genes positively correlates with increased RNA Pol-II density and transcriptional outputs. The results suggest that Smyd3 is an essential transcriptional potentiator of a multitude of cancer-related genes. Overall design: Standard Smyd3-deficient (Smyd3-KO) mice were generated using gene-trap ES cell clones (AS0527 from International Gene Trap Consortium), in which a selection cassette, containing the splice acceptor site from mouse EN2 exon 2 followed by the beta-galactosidase and neomycin resistance gene fusion gene and the SV40 polyadenylation sequence was inserted into the 5th intron of the Smyd3 gene. The resulting mice were devoid of Smyd3 mRNA and protein in all tissues, including liver and colon. For the generation of Smyd3-Tg mice the open reading frame of the mouse Smyd3 cDNA, which contained 3 Flag epitopes at the 3’ end was inserted into the StuI site of the pTTR1-ExV3 plasmid (Yan et al, 1990). The 6.8 kb HindIII fragment containing the mouse transthyretin enhancer/promoter, intron 1, Smyd3 cDNA, three Flag epitopes and SV40 poly-A site was used to microinject C57Bl/6 fertilized oocytes. Founder animals were identified by Southern blotting and crossed with F1 mice to generate lines. Specific overexpression in the liver was tested by RT-PCR analysis in different tissues.
Publication Title
Smyd3 Is a Transcriptional Potentiator of Multiple Cancer-Promoting Genes and Required for Liver and Colon Cancer Development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The unique metabolic profile of most cancers (aerobic glycolysis) might confer apoptosis-resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential and low expression of the K+ channel Kv1.5, both contributing to apoptosis-resistance. Dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases mitochondrial membrane potential, increases mitochondrial-H2O2 and activates Kv channels in all cancer, but not normal cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation and tumor growth in vitro and in vivo, without apparent toxicity. Molecular inhibition of PDK2 by siRNA mimics DCA. The mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a novel selective anticancer agent.
Publication Title
A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth.
Sample Metadata Fields
No sample metadata fields
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