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Gene expression data from cultured cortical neurons.

ABSTRACT: We used Affymetrix DNA arrays to investigate the extent to which nuclear HDAC4 accumulation affects neuronal gene expression. Cultured neurons were infected with lentiviruses expressing either wildtype HDAC4 or the constitutuvely nuclear 3SA mutant under the control of neuronal Synapsin promoter.

ORGANISM(S): Mus musculus

PROVIDER: GSE41220 | GEO | 2012/11/10

SECONDARY ACCESSION(S): PRJNA176221

REPOSITORIES: GEO

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Gene expression data from cultured cortical neurons.

Project description:We used Affymetrix DNA arrays to investigate the extent to which nuclear HDAC4 accumulation affects neuronal gene expression. Cultured neurons were infected with lentiviruses expressing either wildtype HDAC4 or the constitutuvely nuclear 3SA mutant under the control of neuronal Synapsin promoter. Neurons were infected at 5 days after plating (5DIV) and analyzed at 14 DIV.

2012-11-10 | E-GEOD-41220 | biostudies-arrayexpress

Ubiquitinated proteome of E15.5 murine cortical neurons

Project description:TRIM9 and TRIM67 are neuronally-enriched E3 ubiquitin ligases essential for neuronal morphogenesis and responses to the axon guidance cue netrin-1. Deletion of either gene in the mouse results in subtle neuroanatomical anomalies yet overt deficits in spatial learning and memory. The identify of few TRIM9 or TRIM67 substrates are known. Here we performed ubiquitin remnant profiling approach (Xu et al., 2010)in cultured cortical neurons from murine wildtype, Trim9-/-, Trim67-/-, and Trim9-/-:Trim67-/- embryos cultured with or without netrin-1 supplementation to attempt to identify proteins with altered ubiquitination. Although batch variability hindered our ability to identify differential protein ubiquitination, the results delineate the neuronal ubiquitionome during neurite outgrowth, axon specification, and axon branching.

2021-01-04 | PXD021818 | Pride

Effect of Environmental Enrichment on Transcriptomic Profile and Chromatin Accessibility of Cortical Neurons

Project description:Wildtype Swiss webster mice were exposed to four weeks of either standard housing (SH) or environmental enrichment (EE) starting at one month of age. EE chambers were large mouse cages containing two nesting/burrowing materials, a running wheel, and toys that were changed every 3-4 days for novelty and exploration. By contrast, SH control mice were housed with an equal number of littermates in smaller, standard cages containing only one nesting material and no toys or running wheel. We used an antibody for Rbfox3 (NeuN) to sort neuronal nuclei from the dissociated frontal cortices of male mice reared in EE and SH conditions. Isolated neuronal nuclei were then subjected to ATAC-seq or nuclear RNA isolation (random hexamer priming) as per published protocols.

2021-11-17 | GSE176435 | GEO

Effect of inhaled anesthetic to cultured cortical neurons

Project description:Inhaled anesthetics produce many effects and bind to a large number of brain proteins, but it is not yet clear if this is accompanied by widespread changes in gene expression of the biological targets. Such changes in expression might implicate functionally important targets from the large pool of binding targets. Isolated primary cortical neurons were exposed to anesthetics and DNA oligonucleotide microarrays were used to detect and quantify transcriptional changes in neuronal tissue. Keywords: DNA Oligonucleotide Array

2005-07-23 | GSE2982 | GEO

The age and genomic integrity of neurons after cortical stroke in humans

Project description:It has been unclear whether ischemic stroke induces neurogenesis or neuronal DNA-rearrangements in the human neocortex. We show here that neither is the case, using immunohistochemistry, transcriptome-, genome- and ploidy-analyses, and determination of nuclear bomb test-derived 14C-concentration in neuronal DNA. A large proportion of cortical neurons display DNA-fragmentation and DNA-repair short time after stroke, whereas neurons at chronic stages after stroke show DNA-integrity, demonstrating the relevance of an intact genome for survival. Analyze of potential fusion transcripts in 13 samples, seven cortical ischemic stroke tissue and six control cortex, by deep sequencing using Illumina HiSeq 2000

2014-03-28 | E-GEOD-56267 | biostudies-arrayexpress

Dynamic changes in proteome and phosphoproteome following glutamate excitotoxicity in cultured primary cortical neurons

Project description:Excitotoxicity caused by over-stimulation of the ionotropic glutamate receptors is a key neuronal cell death process underpinning brain damage in acute and chronic neurological disorders such as ischaemic stroke, traumatic brain injury, and neurodegenerative diseases. Exactly how neurons die in excitotoxicity still remains unclear and is an important area of research in the field of neuroscience. In this current project we wanted to explore the global changes in proteome and phosphoproteome following glutamate excitotoxicity in cultured primary cortical neurons.

2019-03-07 | PXD008353 | Pride

ChIP-seq analysis about Hdac4/5 samples

Project description:To identify whether Hdac4/5 were enriched in MuERVL directly, we performed Hdac4/5 ChIP-seq with anti-Hdac4/5 antibody in wildtype ESCs. we conclude that Hdac4/5 binding were enriched on MuERVL-int region and weakly enriched on MT2, suggesting a direct regulatory role of Hdac4/5 on MuERVL expression.

2022-09-05 | GSE178130 | GEO

Nuclear SLIC-CAGE of human cortical neurons from Cornelia de Lange Syndrome patients and control individuals

Project description:We used SLIC-CAGE to map transcriptional start sites in cortical neurons from Cornelia de Lange Syndrome (CdLS) patients and control individuals. SLIC-CAGE was performed using nuclear RNA isolated from pre-frontal cortical grey matter. Usage of nuclear RNA allows enrichment of unstable RNAs, such as RNA originating from enhancer transcription. We characterised promoter-level gene expression in cortical neurons from CdLS patients and found deregulation of hundreds of genes enriched for neuronal functions.

2021-02-27 | E-MTAB-9045 | biostudies-arrayexpress

Single cell sequencing of iPSC-dopamine neurons reconstructs disease progression and identifies HDAC4 as a regulator of Parkinson cell phenotypes

Project description:Induced pluripotent stem cell (iPSC)-derived dopamine neurons provide an opportunity to model Parkinson’s disease (PD) but neuronal cultures are confounded by cellular heterogeneity. By applying high-resolution single cell transcriptomic analyses to Parkinson’s iPSC-derived dopamine neurons carrying the GBA-N370S risk variant, we exploited intra-culture cellular heterogeneity to identify a progressive axis of gene expression variation leading to endoplasmic reticulum stress. Analysis of genes differentially-expressed (DE) along this axis identified the transcriptional repressor histone deacetylase 4 (HDAC4) as an upstream regulator of disease progression. HDAC4 was mislocalized to the nucleus in PD iPSC-derived dopamine neurons and repressed genes early in the disease axis, leading to late deficits in protein homeostasis. Treatment of iPSC-derived dopamine neurons with compounds known to modulate HDAC4 activity upregulated genes early in the DE axis, and corrected Parkinson’s-related cellular phenotypes. Our study demonstrates how single cell transcriptomics can exploit cellular heterogeneity to reveal disease mechanisms and identify therapeutic targets.

2018-10-17 | E-MTAB-7303 | biostudies-arrayexpress

PRR7 is a novel NMDA-dependent inhibitor of c-Jun ubiquitination in neurons

Project description:Elevated c-Jun levels result in apoptosis and are evident in neurodegenerative disorders such as Alzheimer's disease and dementia and after global cerebral insults such as stroke and epilepsy. NMDA receptor (NMDAR) antagonists block c-Jun upregulation and prevent neuronal cell death following excitotoxic insults. However, little is known about the molecular mechanisms that regulate c-Jun abundance in neurons. Here we show that PRR7, a component of synaptic junctions, can upregulate c-Jun levels by inhibiting its ubiquitination in neurons. PRR7 interacts with the GLUN1 subunit of NMDARs and is upregulated in the nucleus following NMDAR activation. We show that PRR7 interacts with the E3 ligase SCFFBW7 (FBW7) and blocks the FBW7-mediated ubiquitination of c-Jun. PRR7 overexpression increases c-Jun-dependent transcriptional activity and promotes neuronal death. Microarray assays indicate that both Prr7 knockdown or overexpression alter the abundance of c-Jun-regulated transcripts associated with cellular viability as well as synaptic function. Moreover, Prr7 knockdown attenuates NMDA-mediated excitotoxicity in primary neuronal cultures. Our results show that PRR7 links NMDAR activity to c-Jun function and provide insight into the processes that underlie NMDA-dependent excitotoxicity. Four biological replicas of each of the four conditions: NO = not transduced with virus; NT = transduced with control lentiviruses containing a non-targeting shRNA sequence; KD = transduced with lentiviruses expressing PRR7-specific shRNAs; OE= transduced with lentiviruses to overexpress PRR7.

2014-10-25 | E-GEOD-62686 | biostudies-arrayexpress

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