Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional dysregulation in a primary cortical neuron model of Huntington's disease

ABSTRACT: Transcriptional dysregulation in a primary cortical neuron model of Huntington's disease

PROVIDER: PRJNA475261 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional dysregulation in a primary cortical neuron model of Huntington's disease

Project description:Transcriptional dysregulation in a primary cortical neuron model of Huntington's disease

2018-06-09 | GSE115522 | GEO

TRE-Htt-N853 Huntington's Disease in vitro model

Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study

2008-09-01 | GSE12481 | GEO

Cortical astroglia transcriptomic dysregulation in the G93A SOD1 ALS mouse model

Project description:Astroglia are the most abundant cell type in the central nervous system. They play essential roles in the homeostasis of the CNS. Astroglia are extremely diverse. In Amyotrophic Lateral Sclerosis (ALS) astroglia in spinal cord undergo dramatic transcriptomic dysregulation. However there is little to no data on the effects that cortical astroglia undergo during ALS pathogenesis. In this study we isolated pure cortical astroglia in end stage ALS mice. We performed microarray analysis and discovered dysregulated pathways and genetic markers. This may serve as a database for scientists to understand the effects that abnormal cortical astroglia have on cortical motor neurons and overall ALS pathology.

2019-04-30 | GSE111031 | GEO

N-terminomics Analysis of Mouse cultured cortical neuron during excitotoxicity

Project description:Excitotoxicity is a primary pathological process directing neuronal cell death in both acute neurological disorders and neurodegenerative diseases such as ischemic stroke and Alzheimer’s disease. We use mouse cultured cortical neuron treated with 100uM of Glutamate for a model of excitotoxicity and applied N-terminomics (TAILS) method to identify the neuronal proteins aberrantly modified in excitotoxicity

2023-04-07 | PXD040648 | Pride

sFANS RNAseq profiling of deep layer cortical cell types from human control and Huntington's Disease samples

Project description:The properties of the cell types that are most vulnerable in the Huntington's disease (HD) cortex have not been delineated. Here we have employed serial fluorescence activated nuclear sorting (sFANS) and deep molecular profiling to demonstrate that layer 5a pyramidal neurons are selectively vulnerable in primary motor cortex and other cortical areas.

2024-01-17 | GSE233408 | GEO

Cortical astroglia transcriptomic dysregulation in the G93A SOD1 ALS mouse model

Project description:Cortical astroglia transcriptomic dysregulation in the G93A SOD1 ALS mouse model

| PRJNA435616 | ENA

Expression profiles of primary cortical neurons after knocking down Fus

Project description:To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary cortical neuron infected with lentivirus expressing shRNA against mouse Fus or control. RNA was harvested 11 days after transfection.

2012-07-23 | E-GEOD-36153 | biostudies-arrayexpress

Transcription profiling of rat striatal neuron cultures infected with TRE-Htt-N853 - Huntingtons Disease in vitro model

2008-10-25 | E-GEOD-12481 | biostudies-arrayexpress

Restoration of Progranulin Expression Rescues Cortical Neuron Generation in Induced Pluripotent Stem Cell Model of Frontotemporal Dementia

Project description:To understand how haploinsufficiency of progranulin (PGRN) protein causes frontotemporal dementia (FTD), we created induced pluripotent stem cells (iPSC) from patients carrying the GRNIVS1+5G>C mutation (FTD-iPSCs). FTD-iPSCs were fated to cortical neurons, the cells most affected in FTD and known to express PGRN. Although generation of neuroprogenitors was unaffected, their further differentiation into neurons, especially CTIP2-, FOXP2- or TBR1-TUJ1 double positive cortical neurons, was significantly decreased in FTD-neural progeny. Zinc finger nuclease-mediated introduction of PGRN cDNA into the AAVS1 locus corrected defects in cortical neurogenesis, demonstrating that PGRN haploinsufficiency causes inefficient cortical neuron generation. RNAseq analysis confirmed reversal of altered gene expression profile following genetic correction. Wnt signaling pathway, one of the top defective pathways in FTD-iPSC-derived neurons coupled with its reversal following genetic correction, makes it an important candidate. Therefore, we demonstrate for the first time that PGRN haploinsufficiency hampers corticogenesis in vitro.

2014-11-12 | GSE60902 | GEO

Expression profiles of primary cortical neurons after knocking down Cugbp1

Project description:To clarify the functional properties of Cugbp1, we established the differentially expressed alternative exons in Cugbp1-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Cugbp1 or control. RNA was harvested 11 days after transfection.

2013-04-18 | E-GEOD-46147 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data