E-MTAB-7836
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-7836 | ExpressionAtlas | 2019-09-09
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-7836-analysis-methods.tsv | Tabular | |||
| E-MTAB-7836-analytics.tsv | Tabular | |||
| E-MTAB-7836-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-7836-configuration.xml | Xml | |||
| E-MTAB-7836-g2_g1-mvaPlot.png | Other |
Items per page: 5 1 - 5 of 22 |
Similar Datasets
Project description:Gene-expression changes in neurons active during contextual fear conditioning compared to controls left in the homecage
| PRJEB31967 | ENA
Project description:This experiment uses a transgenic mouse that allows for activity-induced expression of an HA-tagged ribosome in an inducible and cre-dependent manner. This allowed us to assess long-lasting gene-expression changes in neurons active during contextual fear conditioning. Previous studies have used similar systems to look a transient changes in gene expression in these neurons, but we developed a system to look at long lasting changes. The workflow includes tissue dissection of the prefrontal cortex, tissue homogenization followed by an immunoprecipitation of the tagged ribosomes using antibodies against HA. RNA bound to the ribosomes is then purified, a cDNA library is prepared and RNAseq was performed. The experimental group was fear conditioned and the control group was left in their homecage for induction of HA- expression in active neurons.
2020-03-27 | E-MTAB-7836 | biostudies-arrayexpress
Project description:Gene expression of RonTK-/- mammary glands compared to RonTK+/+ controls during development
| PRJNA117343 | ENA
Project description:In order to obtain an overview of gene expression changes in CHMP2B-dependent frontotemporal dementia (FTD3), RNA sequencing analyses were performed in FTD3 patient neurons compared to their gene-corrected isogenic controls.
2017-06-12 | GSE92340 | GEO
Project description:Transforming growth factor (TGF) plays an important role in tooth morphogenesis and mineralization. During postnatal development, the dental pulp (DP) mesenchyme secretes neurotrophic factors that guide trigeminal nerve fibers into and throughout the DP. This process is tightly linked with dentin formation and mineralization. Our laboratory established a mouse model in which Tgfbr2 was conditionally deleted in DP mesenchyme using an Osterix promoter-driven Cre recombinase (Tgfbr2cko). These mice survived postnatally with significant defects in bones and teeth, including reduced mineralization and short roots. Hematoxylin and eosin staining revealed reduced axon-like structures in the mutant mice. Reporter imaging demonstrated that Osterix-Cre activity within the tooth was active in the DP and derivatives, but not in neurons. Immunofluorescence staining for 3 tubulin (neuronal marker) was performed on serial cryosections from control and mutant molars on postnatal days 7 and 24 (P7, P24). Confocal imaging and pixel quantification demonstrated reduced innervation in Tgfbr2cko first molars at both stages compared to controls, indicating that signals necessary to promote neurite outgrowth were disrupted by Tgfbr2 deletion. We performed mRNA-Sequence (RNA-Seq) and gene onotology analyses using RNA from the DP of P7 control and mutant mice to investigate the pathways involved in Tgfbr2-mediated tooth development. These analyses identified downregulation of several mineralization-related and neuronal genes in the Tgfbr2cko DP compared to controls. Select gene expression patterns were confirmed by quantitative real-time PCR and immunofluorescence imaging. Lastly, trigeminal neurons were co-cultured atop Transwell filters overlying primary Tgfbr2f/f DP cells. Tgfbr2 in the DP was deleted via adenovirus-expressed Cre recombinase. Confocal imaging of axons through the filter pores showed increased axonal sprouting from neurons cultured with Tgfbr2-positive DP cells compared to neurons cultured alone. Axon sprouting was reduced when Tgfbr2 was knocked down in the DP cells. Immunofluorescence of dentin sialophosphoprotein in co-cultured DP cells confirmed reduced mineralization potential in cells with Tgfbr2 deletion. Both our proteomics and RNA-Seq analyses indicate that axonal guidance cues, particularly semaphorin signaling, were disrupted by Tgfbr2 deletion. Thus, Tgfbr2 in the DP mesenchyme appears to regulate differentiation and the cells’ ability to guide neurite outgrowth during tooth mineralization and innervation.
2022-02-04 | PXD031046 | Pride
Project description:We investigated changes in gene expression of dorsal root ganglia (DRG) isolated from global (pCAGG-CreER x Nav1.7 floxed) Nav1.7 knockout mice using bulk RNA sequencing. We found an upregulation of Penk and downregulation of Ceacam10 in Nav1.7 knockouts compared to controls, as well as other gene expression changes similar to those previously reported for Nav1.7 knockout mice (https://doi.org/10.1038/ncomms9967). We identified that genes selectively expressed in the C low-threshold mechanoreceptor (cLTMR) class of DRG neurons showed a general reduction in expression in Nav1.7 knockouts compared to littermate controls.
2023-05-22 | GSE213826 | GEO
Project description:Cellular differentiation requires cells to undergo dramatic but strictly controlled changes in chromatin organization, transcriptional regulation, and protein production and interaction. To understand the regulatory connections between these processes, we applied a multi-omics approach integrating proteomic, transcriptomic, chromatin accessibility, protein occupancy, and protein-chromatin interaction data acquired during differentiation of mouse embryonic stem cells (ESCs) into post-mitotic neurons. We found extensive remodeling of the chromatin that was preceding changes on RNA and protein levels. We found the pluripotency factor Sox2 as regulator of neuron-specific genes and, as a potential mechanism, revealed its genomic redistribution from pluripotency enhancers to neuronal promoters and concomitant change of its protein interaction network upon differentiation. We identified Atrx as a major Sox2 partner in neurons, whose co-localisation correlated with an increase in active enhancer marks and increased expression of nearby genes, and where deletion of a Sox2-Atrx co-bound site resulted in reduced expression of the proximal gene. Collectively, these findings provide key insights into the regulatory transformation of Sox2 during neuronal differentiation and highlight the significance of multi-omic approaches in understanding gene regulation in complex systems.
2020-06-04 | PXD016080 | Pride
Project description:Neural stem cells derived from early-onset Alzheimer’s disease (EOAD) patients with PSEN1 mutations, late-onset Alzheimer’s disease (LOAD) patients with APOE4 genotypes, and sex-matched wild-type (WT) controls were cultured and differentiated to neurons. Undifferentiated cells (UD, cultured for 1 day) and differentiated cells (DIF, cultured for 35 days) were compared to study gene expression changes. Oligomeric amyloid beta (Aβ, 0.5 µM) was applied to differentiated WT neurons for 24 hours prior to RNA sequencing. Differential gene expression analysis revealed that genetic background differences between healthy controls, as well as between EOAD and LOAD, contribute as many expression changes as AD-specific mutations. Comparing differentiation-induced gene expression changes between AD neurons and corresponding healthy controls circumvents background variability and highlights disease-specific alterations.Analysis of over 100 AD-associated genes showed altered expression in differentiated EOAD and LOAD neurons, consistent with roles in neuronal functions and AD etiopathogenesis. Notably, LOAD neurons, but not EOAD neurons, exhibited significant deficiencies in heme and redox homeostasis, with reduced expression of genes associated with heme metabolism, oxidative phosphorylation, and NAD/NADH homeostasis. These deficiencies may underlie neuronal dysfunction and contribute to LOAD pathogenesis. Gene Ontology enrichment analysis identified pathways uniquely dysregulated in EOAD and LOAD, offering insights into the molecular mechanisms distinguishing these forms of Alzheimer’s disease. This study emphasizes the critical role of redox and heme homeostasis in LOAD and identifies gene expression patterns altered specifically by AD mutations.
2025-09-21 | GSE288917 | GEO
Project description:To investigate gene expression changes related to two fAD mutations (A79V and L150P) in the Presenilin-1 gene (PSEN1) we compared the transcriptomes (polyA and total) of glutamatergic cortical neurons derived from fAD-mutant human induced pluripotent stem cells and their individual isogenic controls generated via precision CRISPR/Cas9 genome editing.
2023-01-24 | GSE211993 | GEO
Project description:16p13.11 copy number variants (CNVs) have been associated with autism, schizophrenia, psychosis, intellectual disability, and epilepsy. The majority of 16p13.11 deletions or duplications occur within three well-defined intervals, and despite growing knowledge of the functions of individual genes within these intervals, the molecular mechanisms that underlie commonly observed clinical phenotypes remain largely unknown. Patient-derived, induced pluripotent stem cells (iPSCs) provide a platform for investigating the morphological, electrophysiological, and gene-expression changes that result from 16p13.11 CNVs in human-derived neurons. Patient derived iPSCs with varying sizes of 16p13.11 deletions and familial controls were differentiated into cortical neurons for phenotypic analysis. High-content imaging and morphological analysis of patient-derived neurons demonstrated an increase in neurite branching in patients compared with controls. Whole-transcriptome sequencing revealed expression level changes in neuron development and synaptic-related gene families, suggesting a defect in synapse formation. Subsequent quantification of synapse number demonstrated increased numbers of synapses on neurons derived from early-onset patients compared to controls. The identification of common phenotypes among neurons derived from patients with overlapping 16p13.11 deletions will further assist in ascertaining common pathways and targets that could be utilized for screening drug candidates. These studies can help to improve future treatment options and clinical outcomes for 16p13.11 deletion patients.
2024-06-23 | GSE208574 | GEO