Expression data from DMSO and SP600125 treated neurons
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ABSTRACT: Expression profiling of from DMSO and SP600125 treated glutamatergic neurons reveals JNK target genes that are transcriptionally regulated by JNK signaling. SP600125 is a known JNK signaling inhibitor and therefore, we used this to test whether the expression of JNK bound genes is affected upon inhibition of JNK kinase activity. Gene expression in the SP600125 treated neurons was compared to the DMSO treated neurons. a to e suffixes indicate biological replicates. Batch indicates different batches of the drug SP600125.
Project description:This SuperSeries is composed of the following subset Series: GSE25529: Expression data from DMSO and SP600125 treated neurons GSE25532: NF-Y recruits JNK to Chromatin during Stem Cell Differentiation Refer to individual Series
Project description:Expression profiling of from DMSO and SP600125 treated glutamatergic neurons reveals JNK target genes that are transcriptionally regulated by JNK signaling. SP600125 is a known JNK signaling inhibitor and therefore, we used this to test whether the expression of JNK bound genes is affected upon inhibition of JNK kinase activity.
Project description:Expression profiling of from Top2β knokout and ICRF-193 treated neurons reveals a significant number of genes that are transcriptionally deregulated Gene expression in the Top2β knocnout ES, NP and TN stages of stem cell differention to the corresponidng wild type cells. In vitro derived neurons and cortical glutamatergic neurons were either treated with DMSO or ICRF-193 and were compared to reveal differentially expressed genes.
Project description:This SuperSeries is composed of the following subset Series: GSE27245: Expression data from Top2β KO cells as well ICRF-193 treatment of in vitro derived neurons and cortical glutamatergic neurons GSE27246: Top2β ChIP-chip Refer to individual Series
Project description:While changes in chromatin are integral to transcriptional reprogramming during cellular differentiation, it is currently unclear how chromatin modifications are targeted to specific loci. We developed a computational model on the premise that transcription factors (TFs) direct dynamic chromatin changes during cell fate decisions. When applied to a neurogenesis paradigm, this approach predicted the TF REST as a determinant of gain of Polycomb-mediated H3K27me3 in neuronal progenitor cells. We prove this prediction experimentally by showing that the absence of REST causes loss of H3K27me3 at target promoters in trans at the same cellular state. Moreover, promoter fragments containing a REST binding site are sufficient to recruit H3K27me3 in cis, while deletion of their REST site results in loss of H3K27me3. These findings illustrate that computational modeling can systematically identify TFs that regulate chromatin dynamics genome-wide. Local determination of Polycomb activity by REST exemplifies such TF based regulation of chromatin. Expression profiling of REST knock-out (RESTko) versus REST wildtype (RESTwt) or REST heterozygous knock-out (RESThet) cells at three stages of in vitro neuronal differentiation. RESTko and RESTwt/RESThet embryonic stem (ES) cells were differentiated to terminal neurons (TN) via a defined neuronal progenitor (NP) state. Three biological replicates (suffixes a to c).
Project description:TGF-beta plays multiple functions in a board range of cellular responses such as proliferation, differentiation, motility and survival by activating several cellular signaling pathways, including Smads and MAP kinases (Erk, JNK and p38). In particular, TGF-beta can activate pro- or anti-apoptotic signals depending on the target cells. We found that blockage of JNK activation sensitized mouse B lymphoma derived A20 cells to TGF-beta-induced apoptosis. These results suggest that TGF-beta activate JNK to inhibit the activation of death signal that is simultaneously activated by TGF-beta. We used microarrays to gain insight into the effects of JNK inhibition on gene expression in TGF-b-stimulated A20 cells and identified JNK-dependent TGF-beta inducible genes. Experiment Overall Design: The following six samples were prepared: untreated A20 cells (non-stimulated, DMSO): A20 cells cultured with SP600125 for 24 h (non-stimulated, SP600125): A20 cells stimulated with TGF-beta for 12 h (TGF-beta 12 h, DMSO) and 24 h (TGF-beta 24 h, DMSO): and A20 cells stimulated with TGF-beta in the presence of SP600125 for 12 h (TGF-beta 12 h, SP600125) and 24 h (TGF-beta 24 h, SP600125), respectively. Total RNA was prepared and hybridized to the Affymetrix Mouse Genome 430 2.0 array. Genes whose expression was increased by more than 2-fold at either 12 or 24 h after TGF-beta stimulation were identified as TGF-beta inducible genes. Amongst them, we identified genes whose induction levels were reduced by more than 75% by co-treatment with the JNK inhibitor SP600125.
Project description:Transcriptional analysis of identified DRG subpopulations. Cell-type specific intrinsic programs instruct neuronal subpopulations before target-derived factors influence later neuronal maturation. Retrograde neurotrophin signaling controls neuronal survival and maturation of dorsal root ganglion (DRG) sensory neurons, but how these potent signaling pathways intersect with transcriptional programs established at earlier developmental stages remains poorly understood. Here we determine the consequences of genetic alternation of NT3 signaling on genome-wide transcription programs in proprioceptors, an important sensory neuron subpopulation involved in motor reflex behavior. We find that the expression of many proprioceptor-enriched genes is dramatically altered by genetic NT3 elimination, independent of survival-related activities. Combinatorial analysis of gene expression profiles with proprioceptors isolated from mice expressing surplus muscular NT3 identifies an anticorrelated gene set with transcriptional levels scaled in opposite directions. Voluntary running experiments in adult mice further demonstrate the maintenance of transcriptional adjustability of genes expressed by DRG neurons, pointing to life-long gene expression plasticity in sensory neurons. We combined a mouse line expressing GFP under the control of the TrkC promoter (BAC transgene approach) with various NT3 signaling mutants in order to identify the transcriptional changes in identified subpopulations of dorsal root ganglia (DRG) neurons. Sorted cells were processed for RNA extraction and hybridization on Affymetrix microarrays. Analysis was performed a postnatal (p) day p0. Subsequent analysis focused on the transcriptional profile of DRG neuron subpopulations at specific lumbar levels. Additional work addressed the transcriptional changes in whole DRG in adult mice with and without physical exercise.
Project description:We identify mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability. In this data set we compare the expression profile of human HEK293 Flp-In cells stably expressing TRIM71 to that of the parental cells, not expressing TRIM71 protein. Experiment was performed in triplicate.
Project description:We identify mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability. In this data set we compare the expression profile of mouse ES upon Trim71 KD versus that of the parental cells. Experiment was performed in triplicate.