Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA132309 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression profiling of HEK293T cells transfected with miR-neg (negative control), miR-132 or miR-381 mimics and treated with forskolin for 0, 1 or 4hrs.
2011-07-01 | GSE24812 | GEO
Project description:Expression profiling of HEK293T cells transfected with miR-neg (negative control), miR-132 or miR-381 mimics and treated with forskolin for 0, 1 or 4hrs. HEK293T cells were reverse transfected with the respective miRNA mimics. 72hrs post-transfection, cells were treated with forskolin for 0, 1 or 4hrs. Total RNA was then extracted. Expression profiling was carried out with Affymetrix arrays. Experiment was performed in duplicate. Total of 18 samples.
2011-07-01 | E-GEOD-24812 | biostudies-arrayexpress
Project description:The expression of different RNAs in miR-124/miR-132 transfected HEK293T cells were compared to mock treated samples in order to describe fold change of transcripts assigned as miRNA targets by different tools or experiments.
2020-11-23 | E-MTAB-8516 | biostudies-arrayexpress
Project description:Targetome of miR-124/miR-132 was enriched in HEK293T cells, a cell line which lacks the expression of these miRNA. The targetome was captured using miR-CLIP, a transfection-based double-purification crosslinking and immunoprecipitation (CLIP) method. Therefore HEK293T cells were transfected with miR-124/miR-132 miR-CLIP probes, which are trioxsalen, biotin bis-modified pre-miRNAs. Unspecific RNA-protein and trioxsalen mediated RNA-RNA crosslinking were induced by UV-irradiation before cell lysis. Total RNA (input samples) was enriched for AGO2-bound RNA using AGO2 immunoprecipitation, by depleting non-RISC associated RNAs. A second enrichment for specific targets of the transfected miRNA is performed using magnetic streptavidin-beads. This step relies on the interaction of the biotinylated probe, on which the RNA target is crosslinked, with the beads. The method was shown to deliver high-quality miRNA targetomes of both 5p and 3p miRNAs.
2020-11-23 | E-MTAB-8517 | biostudies-arrayexpress
Project description:The CREB family of transcription factors stimulates cellular gene expression following phosphorylation at a conserved serine (Ser133 in CREB1) in response to cAMP and other extracellular signals. In order to characterize CREB target genes in various tissues, we give a cAMP agonist, forskolin (FSK), to cell lines or primary cultures and monitor the gene expression. To eliminate CREB-independent effects of FSK on cellular gene expression, we employed a dominant negative form of CREB called A-CREB, which dimerizes selectively with and blocks the DNA binding activity of CREB but not other bZIP family members. Therefore, genes that are induced by cAMP and the induction was blocked by A-CREB treatment likely represents CREB target genes. Notes:; 1) In HEK293T cells, besides the Control+FSK+(FSK-ACREB) experiments, a different set of experiments showing FSK effect on 1hr and 4hr is included. The two sets of data in HEK293T were generated at different times with different batch of cells, and comparison should be limited within each set. The cAMP induced genes at 1hr, however, was similar between the two sets. 2) These is no ACREB data for pancreatic islets or hepatocytes. For hepatocytes, however, we have included fasting liver and refed liver in additional to FSK treated primary hepatocytes. During fasting, glucagon induces cAMP increase in the liver and CREB is activated. Therefore, a more reliable list of CREB target genes in hepatocytes can be obtained by selecting those genes are that induced both during fasting and in FSK treated primary culture.
2008-06-12 | E-GEOD-2060 | biostudies-arrayexpress
Project description:The CREB family of transcription factors stimulates cellular gene expression following phosphorylation at a conserved serine (Ser133 in CREB1) in response to cAMP and other extracellular signals. In order to characterize CREB target genes in various tissues, we give a cAMP agonist, forskolin (FSK), to cell lines or primary cultures and monitor the gene expression. To eliminate CREB-independent effects of FSK on cellular gene expression, we employed a dominant negative form of CREB called A-CREB, which dimerizes selectively with and blocks the DNA binding activity of CREB but not other bZIP family members. Therefore, genes that are induced by cAMP and the induction was blocked by A-CREB treatment likely represents CREB target genes. Notes: 1) In HEK293T cells, besides the Control+FSK+(FSK-ACREB) experiments, a different set of experiments showing FSK effect on 1hr and 4hr is included. The two sets of data in HEK293T were generated at different times with different batch of cells, and comparison should be limited within each set. The cAMP induced genes at 1hr, however, was similar between the two sets. 2) These is no ACREB data for pancreatic islets or hepatocytes. For hepatocytes, however, we have included fasting liver and refed liver in additional to FSK treated primary hepatocytes. During fasting, glucagon induces cAMP increase in the liver and CREB is activated. Therefore, a more reliable list of CREB target genes in hepatocytes can be obtained by selecting those genes are that induced both during fasting and in FSK treated primary culture. Keywords: parallel sample
2005-03-02 | GSE2060 | GEO
Project description:We overexpressed miR-212/132 by AAV9 in mouse model of doxorubicin-induced cardiotoxicity and wanted to identify myocardial targets of miR-212/132 in this model.
2018-12-29 | GSE121965 | GEO
Project description:Transcriptomic profiling of miR-132/212-deficient and WT CD4 T cells isolated from spleens of L donovani infected mice (d28) to determine the effects of miR-132/212 on CD4 T cell activation in vivo. This was combined by transcriptomic analysis of early stage in vitro activated WT and miR-132/212-deficient CD4 T cells to identify direct miR-132/212 targets in CD4 T cells.
2019-03-22 | GSE125268 | GEO
Project description:The abnormal regulation of amyloid-b (Ab) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimerâs disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Ab deposition and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Ab metabolism, including Tau, Mapk, and Sirt1. We used RNA-Seq to analyse the hippocampus of 3xTg-AD mice lacking the miR-132/212 cluster as well as Neuro2a cells overexpressing miR-132 mimics.
2016-07-17 | E-GEOD-84481 | biostudies-arrayexpress
Project description:We studied the role of the cAMP responsive factor CREB in promoting insulin resistance following its activation in adipose under obese conditions We identified genes that were upregulated in primary cultures of mouse adipocytes following exposure to forskolin; and we characterized genes that are also induced in white adipose tissue in mice maintained on a high fat diet. Keywords: signaling study
2009-03-03 | GSE14363 | GEO