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GSE45229
Mus musculus
20 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Quetiapine is an atypical neuroleptic with a pharmacological profile distinct from classic neuroleptics. It is currently approved for treating patients with schizophrenia, major depression and bipolar I disorder. However, its cellular effects remain elusive.
Publication Title
Unique pharmacological actions of atypical neuroleptic quetiapine: possible role in cell cycle/fate control.
Sample Metadata Fields
Sex, Treatment
View Samples- Mus musculus
- 477 Downloadable Samples
Illumina HiSeq 2500
Description
Neuronal diversity is a defining feature of the mammalian brain deemed necessary for realizing the complex function of the nervous system. In order to begin to understand the transcriptional basis of this diversity, we collected more than 170 neuronal and non-neuronal cell type-specific transcriptomes defined operationally by transgenic mouse lines and anatomical regions. The dataset indicates that the genes specifically expressed in neuronal cell types are biased toward long genes. We revealed that these long genes have higher capacities to be differentially expressed between cell types and thus assume an important role in diversification of the neuronal transcriptomes. Since mobile element insertions are the main cause of the gene elongations, we propose that exaptation of the inserted mobile elements significantly contributed to the neuronal diversity. Overall design: Examination of whole cell transcriptomes in 174 cell types.
Publication Title
Mapping the transcriptional diversity of genetically and anatomically defined cell populations in the mouse brain.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Argonaute (Ago) proteins, which act in post-transcriptional gene regulation directed by small RNAs, are vital for normal stem cell biology. Here we report the genomic characterization of stable Ago-deficient mouse embryonic stem cells (mESC) and determine the direct, primary and system level response to loss of Ago-mediated regulation. We find mESCs lacking all four Ago proteins are viable, do not repress microRNA (miRNA)-targeted cellular RNAs, and show distinctive gene network signatures. Profiling of RNA expression and epigenetic activity in an Ago mutant genetic series indicates that early responses to Ago loss are driven by transcriptional regulatory networks, in particular the Tgf-ß/Smad transcriptional network. This finding is confirmed using a time course analysis of Ago depletion and Ago rescue experiments. Detailed analysis places Tgf-ß/Smad activation upstream of cell cycle regulator activation, such as Cdkn1a, and repression of the c-Myc transcriptional network. The Tgf-ß/Smad pathway is directly controlled by multiple low-affinity miRNA interactions with Tgf-ß/Activin receptor mRNAs and receptor-mediated activation is required for Tgf-ß/Smad target induction with Ago loss. Our characterization reveals the interplay of post-transcriptional regulatory pathways with transcriptional networks in maintaining cell state and likely coordinating cell state transitions. Overall design: mRNA seq from stable genetic Dicer and Dgcr8 mutant mouse embryonic stem cells.
Publication Title
Temporal Control of the TGF-β Signaling Network by Mouse ESC MicroRNA Targets of Different Affinities.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 36 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Here, we examined mouse brain trancriptional changes 1 hour after the 10th daily i.p. treament with one of the four following treaments: i) vehicle control (45% saline, 45% PEG-400 and 10% DMSO administered at 7.5mL/kg), ii) Cpd-60, 45mg/kg , administered at 7.5mL/kg or iii) SAHA, 25mg/kg, administered at 5mL/kg) or iv) CI-994, 10mg/kg, administered at 5mL/kg. Cpd-60 is a benzamide HDAC inhibitor with selectivity for class I HDAC subtypes HDAC1 and HDAC2; CI-994 is a benzamide inhibitor with selectivity for HDACs1,2 and 3; SAHA is a hydroxamic acid HDAC inhibitor with selectivity for class I HDAC subtypes 1,2, and 3 and the class II HDAC subtype HDAC 6. We examined transcript differences using the Illumnia WG-6 2.0 whole genome expression array and profiled 3 specific brain regions (prefrontal cortex, nucleus accumbens, hippocampus) from each of 36 mice (n=6 mice / treatment group) . For application to array chips, we pooled two biological replicates from like treatment and brain region-groups such that 36 samples were applied in total: 4 treatment groups x 3 brain regions per treament group x 3 pools of two samples each for each treatment/brain region.
Publication Title
A selective HDAC 1/2 inhibitor modulates chromatin and gene expression in brain and alters mouse behavior in two mood-related tests.
Sample Metadata Fields
Sex, Treatment
View Samples- Mus musculus
- 758 Downloadable Samples
- Illumina HiSeq 2500
Description
Genetic variation modulating risk of sporadic Parkinson's disease (PD) has been primarily explored through genome wide association studies (GWAS). However, like many other common genetic diseases, the impacted genes remain largely unknown. Here, we used single-cell RNA-seq to characterize dopaminergic (DA) neuron populations in the mouse brain at embryonic and early postnatal timepoints. These data facilitated unbiased identification of DA neuron subpopulations through their unique transcriptional profiles, including a novel postnatal neuroblast population and substantia nigra (SN) DA neurons. We use these population-specific data to develop a scoring system to prioritize candidate genes in all 49 GWAS intervals implicated in PD risk, including known PD genes and many with extensive supporting literature. As proof of principle, we confirm that the nigrostriatal pathway is compromised in Cplx1 null mice. Ultimately, this systematic approach establishes biologically pertinent candidates and testable hypotheses for sporadic PD, informing a new era of PD genetic research. Overall design: 473 single cell RNA-Seq samples from sorted mouse Th-eGFP+ dopaminergic neurons collected at two timepoints from three distinct brain regions.
Publication Title
Single-Cell RNA-Seq of Mouse Dopaminergic Neurons Informs Candidate Gene Selection for Sporadic Parkinson Disease.
Sample Metadata Fields
Specimen part, Subject
View Samples- Bos taurus
- 12 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
Four mature, non-lactating dairy cattle were transitioned from a high forage diet (HF; 0% grain) to a high grain diet (HG; 65% grain) that was fed for three weeks. Rumen papillae biopsies were performed during the HF baseline (week 0) and after the first (week 1) and third week (week 3) of the grain challenge to create a transcript profile for the the short and long-term adaption of the rumen epithelium during ruminal acidosis.
Publication Title
Bovine rumen epithelium undergoes rapid structural adaptations during grain-induced subacute ruminal acidosis.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Stat5a and Stat5b proteins are highly homologous with greater than 90% amino acid identity and share binding to the palindromic Stat5 consensus sequence, TTCNNNGAA, but individual roles of each transcription factor in breast cancer have not been thoroughly evaluated. To determine the degree of similarity between transcripts modulated by Stat5a and Stat5b proteins in human breast cancer, we utilized genome-wide transcript profiling to identify genes regulated specifically by Stat5a or Stat5b in response to prolactin.
Publication Title
Low levels of Stat5a protein in breast cancer are associated with tumor progression and unfavorable clinical outcomes.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 36 Downloadable Samples
- Illumina HiSeq 2500
Description
We identified that downregulation of RNF20/H2Bub1 is involved in HGSOC progression through altering key immune signaling pathways. The goal of this RNA-seq is to analyze gene expression profile in FTSEC cells (FT190 and FT194 cell lines) with RNF20 knockdown (shRNF20) or control shRNA. Integrating the data from ATAC-seq for same samples, we observed that expression of immune signaling pathways have significantly changed by RNF20/H2Bub1 downregulation. Overall design: mRNA profiles of FT190 and FT194 shRNF20 (RNF20 knockdown) or control shRNA cells were generated by deep sequencing using Illumina HiSeq 2500, in triplicate.
Publication Title
Early Loss of Histone H2B Monoubiquitylation Alters Chromatin Accessibility and Activates Key Immune Pathways That Facilitate Progression of Ovarian Cancer.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 30 Downloadable Samples
- IlluminaHiSeq2000
Description
Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) – the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation. Overall design: RNA-seq profiles of prostate cancer cell lines to understand gene expression associated with enzalutamide treatment
Publication Title
Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of the effect on global gene regulation in epididymal adipose tissue of overexpressing the cytoskeletal tropomyosin, Tm5NM1 to help understand the transcriptional events that lead to increased fat mass in transgenic mice.
Publication Title
Regulation of cell proliferation by ERK and signal-dependent nuclear translocation of ERK is dependent on Tm5NM1-containing actin filaments.
Sample Metadata Fields
Specimen part
View Samples