A great number of studies have investigated changes induced by morphine exposure in gene expression using several experimental models. In this study, we examined gene expression changes during chronic exposure to morphine during maturation and differentiation of zebrafish CNS.
Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine: identification of new genes associated with neuronal function and mu opioid receptor expression.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesCaSR modulation inhibits neuroblastoma growth
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesCaSR modulation inhibits neuroblastoma growth
Cinacalcet inhibits neuroblastoma tumor growth and upregulates cancer-testis antigens.
Specimen part, Treatment
View SamplesWe studied the transcriptional profile in yeast cells in response to heterologous expression of mammalian activated AKT1
Heterologous mammalian Akt disrupts plasma membrane homeostasis by taking over TORC2 signaling in Saccharomyces cerevisiae.
No sample metadata fields
View SamplesWe studied the transcriptional profile in response to acute PtdIns-4,5P2 depletion induced by heterologous expression of a plasma membrane-directed version of mammalian PI3K catalytic subunit (p110-CAAX).
The yeast cell wall integrity pathway signals from recycling endosomes upon elimination of phosphatidylinositol (4,5)-bisphosphate by mammalian phosphatidylinositol 3-kinase.
No sample metadata fields
View SamplesDuring transcription initiation, the TFIIH-kinase Kin28/Cdk7 marks RNA polymerase II (Pol II) by phosphorylating the C-terminal domain (CTD) of its largest subunit. Here we describe a structure-guided chemical approach to covalently and specifically inactivate Kin28 kinase activity in vivo. This method of irreversible inactivation recapitulates both the lethal phenotype and the key molecular signatures that result from genetically disrupting Kin28 function in vivo. Inactivating Kin28 impacts promoter release to differing degrees and reveals a “checkpoint” during the transition to productive elongation. While promoter-proximal pausing is not observed in budding yeast, inhibition of Kin28 attenuates elongation-licensing signals, resulting in Pol II accumulation at the +2 nucleosome and reduced transition to productive elongation. Furthermore, upon inhibition, global stabilization of mRNA masks different degrees of reduction in nascent transcription. This study resolves long-standing controversies on the role of Kin28 in transcription and provides a rational approach to irreversibly inhibit other kinases in vivo. Overall design: Total RNA was collected from wild-type and analog-sensitive Kin28 strains treated with reversible inhibitor 1-NAPP-1, irreversible inhibitor CMK, and solvent control DMSO. Equivalent ratios of S. pombe : S. cerevisiae cells were added to each sample before RNA extraction for normalization of read counts after sequencing. Nascent RNA was purified from total RNA by 4-thiouracil labeling, biotinylation, and streptavidin-pulldown. As a negative control, nascent RNA was also extracted from total RNA from cells that had not been treated with 4-thiouracil.
Engineered Covalent Inactivation of TFIIH-Kinase Reveals an Elongation Checkpoint and Results in Widespread mRNA Stabilization.
Cell line, Treatment, Subject
View SamplesWild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization.
Slt2 MAPK pathway is essential for cell integrity in the presence of arsenate.
No sample metadata fields
View SamplesMechanisms of immune regulation may control proliferation of aberrant plasma cells (PCs) in patients with the asymptomatic monoclonal gammopathy of undetermined significance (MGUS) preventing progression to active multiple myeloma (MM). We investigated the role of CD85j (LILRB1), an inhibitory immune checkpoint for B cell function, in MM pathogenesis.
Loss of the Immune Checkpoint CD85j/LILRB1 on Malignant Plasma Cells Contributes to Immune Escape in Multiple Myeloma.
Specimen part, Cell line
View SamplesTo identify genes expressed in specific developing thalamic nuclei during embryonic stages, a genetic dual labelling strategy was established to mark and isolate the cells. Transcription profiles were determined for the principal sensory thalamic populations by genome-wide analysis.
Genetic Labeling of Nuclei-Specific Thalamocortical Neurons Reveals Putative Sensory-Modality Specific Genes.
Specimen part
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