This SuperSeries is composed of the SubSeries listed below.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part, Treatment
View SamplesIdentification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part, Treatment
View SamplesIdentification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part
View SamplesHomozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis
Krüppel-like factor 5 is essential for blastocyst development and the normal self-renewal of mouse ESCs.
No sample metadata fields
View SamplesTo explore gene expression profiles of cells sensitive to necrosis (such as L929 cells) and those sensitive to apoptosis (such as NIH3T3 cells), we conducted expression microarray analysis of L929 cells and NIH3T3 cells.
Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway.
No sample metadata fields
View SamplesTo better understand the molecular basis of the anticancer effects of acyclic retinoid (ACR), a genome-wide screening was applied to identify novel targets of ACR in human hepatocellular carcinoma (HCC) cells JHH7. Gene expression profiles of JHH7 were measured at 0h, 1h and 4 hours after treatment with1 M All-trans retinoic acid (AtRA) or 10 M ACR. Hierarchical clustering with Wards method of 44,907 genes demonstrated diverse expression changes in HCC cells treated with ACR for 4h. A total of 973 differentially expressed genes in response to ACR by comparing with AtRA for 4h treatments were identified with a fold change more than 2. Then, network analysis was performed on the altered gene expression profiles using Ingenuity Pathways Analysis (IPA) program. The most highly populated networks were associated with the regulation of cell cycle and DNA replication, as ACR is well known to induce apoptosis and suppress cell proliferation in HCC cells. Moreover, networks related with amino acid metabolism, protein synthesis and lipid metabolism, such as the biological network entitled Lipid Metabolism, Small Molecular Biochemistry, Vitamin and Mineral Metabolism were also observed. Of interest, this network contains genes that play critical roles in controlling the development of tissues and organs such as the nuclear orphan receptor nuclear receptor subfamily 2, group F, member 2 (NR2F2), suggesting potential drug targets to prevent/treat HCC.
Metabolome Analyses Uncovered a Novel Inhibitory Effect of Acyclic Retinoid on Aberrant Lipogenesis in a Mouse Diethylnitrosamine-Induced Hepatic Tumorigenesis Model.
Sex, Specimen part
View SamplesThe molecular mechanism by which lncRNAs derived from the promoter region where the transcriptional machinery is assembled regulate the expression of neighboring genes during cell differentiation is largely unknown. Myogenesis process has been studied as a model of cell differentiation. Using this model, we found a novel lncRNA, Myoparr, expressed from the promoter region of myogenin gene, one of the regulators of myogenesis. We show that Myoparr regulates the expression of myogenin in vitro and in vivo. In addition, we identified Ddx17 and hnRNPK as Myoparr-binding-proteins. We compared the Transcriptome profiles of C2C12 cells (mouse myoblast cell line) with or without siRNAs against myogenin, Myoparr, Ddx17, and hnRNPK during myogenesis.
Data describing the effects of depletion of <i>M</i><i>yoparr</i>, <i>myogenin</i>, <i>Ddx17</i>, and <i>hnRNPK</i> in differentiating C2C12 cells.
Specimen part, Cell line
View SamplesInvestigating neuronal and photoreceptor regeneration in the retina of zebrafish has begun to yield insights into both the cellular and molecular means by which this lower vertebrate is able to repair its central nervous system. However, knowledge about the signaling molecules in the local microenvironment of a retinal injury and the transcriptional events they activate during neuronal death and regeneration is still lacking. To identify genes involved in photoreceptor regeneration, we combined light-induced photoreceptor lesions, laser-capture microdissection (LCM) of the outer nuclear layer (ONL) and analysis of gene expression to characterize transcriptional changes for cells in the ONL as photoreceptors die and are regenerated. Using this approach, we were able to characterize aspects of the molecular signature of injured and dying photoreceptors, cone photoreceptor progenitors and microglia within the ONL. We validated changes in gene expression and characterized the cellular expression for three novel, extracellular signaling molecules that we hypothesize are involved in regulating regenerative events in the retina.
Identification of the molecular signatures integral to regenerating photoreceptors in the retina of the zebra fish.
No sample metadata fields
View SamplesA promoter associated lncRNA Myoparr is involved in the regulation of skeletal muscle atrophy caused by denervation. However, the molecular mechanism by which Myoparr regulates the expression of downstream genes in skeletal muscle tissue is largely unknown. Thus, we compared the Transcriptome profiles of denervated tibialis anterior muscles transfected with control or Myoparr shRNA.
Long Non-Coding RNA <i>Myoparr</i> Regulates GDF5 Expression in Denervated Mouse Skeletal Muscle.
Sex, Specimen part, Cell line, Treatment
View SamplesDuring translation elongation, the ribosome ratchets along its mRNA template, incorporating each new amino acid and translocating from one codon to the next. The elongation cycle requires dramatic structural rearrangements of the ribosome. We show here that deep sequencing of ribosome-protected mRNA fragments reveals not only the position of each ribosome but also, unexpectedly, its particular stage of the elongation cycle. Sequencing reveals two distinct populations of ribosome footprints, 28-30 nucleotides and 20-22 nucleotides long, representing translating ribosomes in distinct states, differentially stabilized by specific elongation inhibitors. We find that the balance of small and large footprints varies by codon and is correlated with translation speed. The ability to visualize conformational changes in the ribosome during elongation, at single-codon resolution, provides a new way to study the detailed kinetics of translation and a new probe with which to identify the factors that affect each step in the elongation cycle. Overall design: Ribosome profiling, or sequencing of ribosome-protected mRNA fragments, in yeast. We assay ribosome footprint sizes and positions in three conditions: untreated yeast (3 replicates) and yeast treated with translation inhibitors cycloheximide (2 replicates) and anisomycin (2 biological replicates, one technical replicate). We also treat yeast with 3-aminotriazole to measure the effect of limited histidine tRNAs on ribosome footprint size and distribution (two treatment durations).
Distinct stages of the translation elongation cycle revealed by sequencing ribosome-protected mRNA fragments.
Cell line, Treatment, Subject
View Samples