Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA270576 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We investigated gene expression profiles of Parkinson disease (PD) patient's fibroblasts that were treated by SNCA expression-control RNAi to see adverse effects of the RNAi treatment. The data suggested no significant adverse effects caused by the treatment. Total RNA samples prepared from PD fibroblasts that were treated by SNCA expression-control RNAi and by non-silencing RNAi as a control.
2015-06-08 | E-GEOD-64266 | biostudies-arrayexpress
Project description:We investigated gene expression profiles of Parkinson disease (PD) patient's fibroblasts that were treated by SNCA expression-control RNAi to see adverse effects of the RNAi treatment. The data suggested no significant adverse effects caused by the treatment.
2015-06-08 | GSE64266 | GEO
Project description:Expression data from RNAi SNCA treated human neuroblastoma cell line
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Project description:Gene expression profiles of granulin- and control-treated normal human mammary fibroblasts
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Gene expression profiles for ~20,000 genes using Illumina Homo sapiensRef-8 v2
2010-03-25 | GSE21045 | GEO
Project description:Alpha-synuclein (SNCA) accumulation is a hallmark of Parkinson's disease (PD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB), known collectively as synucleinopathies. Current treatments remain symptomatic without addressing the underlying pathology, so therapies that reduce SNCA expression could modify disease progression. This study examines the translational potential of antisense oligonucleotides (ASOs) targeting SNCA mRNA in a physiologically relevant animal model. SNCA-targeted ASOs were administered intracerebroventricularly to two-month-old bacterial artificial chromosome (BAC) transgenic rats expressing the entire human SNCA gene locus. Forty-five days post-injection, substantial SNCA mRNA and protein decreases were detected across multiple brain regions. Transcriptomic analysis revealed decreased synaptic activity and neuronal gene expression alongside region-specific changes in glial gene profiles. Protein assays identified nuanced modulation of neuroimmune mediators and altered AKT signaling, notably reduced phosphorylation of AKT1S1/PRAS40 in the olfactory bulb and decreased activity in AKT pathway components across other brain regions. Behavioral assessments demonstrated increased mobility, enhanced exploratory behavior, and improved olfactory function in treated rats. These findings provide comprehensive molecular, cellular, and behavioral evidence supporting the advancement of SNCA-targeted ASOs as disease-modifying interventions for PD and related synucleinopathies.
2026-09-23 | GSE293775 | GEO
Project description:Parkinson's Disease (PD) is primarily caused by aggregates of alpha synuclein (SNCA) in dopaminergic neurons of the substantia nigra, but PD is a systemic disease and may lead to PD-associated dementia complex. PD-associated encephalopathy is a late manifestation in PD patients at risk for example owing to mutations of the lysosomal enzyme glucocerebrosidase. Defects of lysosomal waste removal and aggregation of mutant alpha synuclein (SNCA) impacts of the proteome. Here, we studied the proteome of the prefrontal cortex in Pink1-/-SNCA A53T double mutant mice in comparison with their wildtype controls. Pink1-/-SNCA A53T mice carry a loss of function knock-in mutation of PTEN induced kinase (Pink1), plus the human A53T mutation of alpha synuclein (SNCA-A53T) [1, 2]. Homozygous Pink1-/-SNCA A53T double mutant mice were generated by crossing Pink1-/- mice (background: 129/SvEv) with A53T-SNCA-overexpressing PrPmtA mice (background: FVB/N) and then, interbreeding the littermates. Wildtype (WT) control mice are hybrids from a crossbreeding of 129/SvEv and FVB/N mice, which were descended from littermates of the respective single mutant animals. Pink1-/-SNCA A53T mice develop spontaneous motor symptoms at advanced ages, with a progressive incidence above 15 months of age. The phenotype of Pink1-/-SNCA A53T and wildtype control mice was observed during aging. Mice were euthanized at an age of 1-1.5 years (matched with the controls). The cortices were rapidly removed and frozen in liquid nitrogen and processed for label free proteomic analyses.
2025-10-21 | PXD039172 | Pride
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description: Not available
| S-EPMC2531291 | biostudies-literature