Ontology highlight
ABSTRACT:
PROVIDER: PRJNA837335 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19173421.fastq.gz | Fastqsanger.gz | |||
| SRR19173422.fastq.gz | Fastqsanger.gz | |||
| SRR19173423.fastq.gz | Fastqsanger.gz | |||
| SRR19173424.fastq.gz | Fastqsanger.gz | |||
| SRR19173425.fastq.gz | Fastqsanger.gz |
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Project description:Differential transcriptome analysis in LUHMES cells overexpressing human wild-type alpha-synuclein or GFP
2022-03-31 | GSE191302 | GEO
Project description:Analysis of striatal transcriptome in transgenic mice overexpressing human wild-type alpha-synuclein
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Project description:Alpha synuclein (SNCA) has been linked to neurodegenerative diseases (synucleinopathies) that include Parkinson’s disease (PD). Although the primary neurodegeneration in PD involves nigrostriatal dopaminergic neurons, more extensive yet regionally selective neurodegeneration is observed in other synucleinopathies. Furthermore, SNCA is ubiquitously expressed in neurons and numerous neuronal systems are dysfunctional in PD. Therefore it is of interest to understand how overexpression of SNCA affects neuronal function in regions not directly targeted for neurodegeneration in PD. To gain a better understanding of the consequences of excessive SNCA expression on basal ganglia function, we performed transcriptome analysis of striatal tissue from male Thy1-aSyn-mice and wt littermates. The present study investigated the consequences of SNCA overexpression on cellular processes and functions in the striatum of mice overexpressing wild-type, human SNCA under the Thy1 promoter (Thy1-aSyn mice) by transcriptome analysis. The analysis revealed alterations in multiple biological processes in the striatum of Thy1-aSyn mice, including synaptic plasticity, signaling, transcription, apoptosis, and neurogenesis. The present study investigated the consequences of SNCA overexpression on cellular processes and functions in the striatum of mice overexpressing wild-type, human SNCA under the Thy1 promoter (Thy1-aSyn mice) by transcriptome analysis. The analysis revealed alterations in multiple biological processes in the striatum of Thy1-aSyn mice, including synaptic plasticity, signaling, transcription, apoptosis, and neurogenesis.
2012-02-11 | GSE35723 | GEO
Project description:Alpha-synuclein is an abundant protein implicated in synaptic function and plasticity, but the molecular mechanism of its action is not understood. Missense mutations and gene duplication/triplication events result in Parkinson's disease, a neurodegenerative disorder of old age with impaired movement and emotion control. Here, we systematically investigated the striatal as well as the cerebellar transcriptome profile of alpha-synuclein-deficient mice via a genome-wide microarray survey in order to gain hypothesis-free molecular insights into the physiological function of alpha-synuclein. A genotype-dependent, specific and strong downregulation of forkhead box P1 (Foxp1) transcript levels was observed in all brain regions from postnatal age until old age and could be validated by qPCR. In view of the co-localization and heterodimer formation of FOXP1 with FOXP2, a transcription factor with a well established role for vocalization, and the reported regulation of both alpha-synuclein and FOXP2 expression during avian song learning, we performed a detailed assessment of mouse movements and vocalizations in the postnatal period. While there was no difference in isolation-induced behavioral activity in these animals, the alpha-synuclein-deficient mice exhibited an increased production of isolation-induced ultrasonic vocalizations (USVs). This phenotype might also reflect the reduced expression of the anxiety-related GABA-A receptor subunit gamma 2 (Gabrg2) we observed. Taken together, we identified an early behavioral consequence of alpha-synuclein deficiency and accompanying molecular changes, which supports the notion that the neural connectivity of sound or emotion control systems is affected. Factorial design comparing SNCA knock-out mice with wild type littermates in two different tissues (striatum, cerebellum) at two different timepoints (6 and 21 month)
2010-07-21 | E-GEOD-19534 | biostudies-arrayexpress
Project description:In order to investigate the effect of Alpha-Ketoglutarate (AKG) on p-α-synuclein in substantia nigra of Parkinson's disease (PD) model mice (C57BL/6), we profiled substantia nigra from wild-type (WT), AAV-α-synuclein (α-Syn), AKG and α-Syn-AKG in male mice by RNA sequencing (RNA-seq).
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Project description:Neurotransmitter release occurs through exocytosis of synaptic vesicles. α-Synuclein’s function and dysfunction in Parkinson’s disease and other synucleinopathies is tightly linked to synaptic vesicle binding. Age is the biggest risk factor for synucleinopathy, and ~15% of synaptic vesicle proteins are linked to diseases of the central nervous system. Yet, age- and disease-induced changes in synaptic vesicles remain unexplored. For an unbiased analysis of the synaptic vesicle proteome, we applied quantitative mass spectrometry to crude synaptic vesicles isolated at three time points (1 month, 3 months, and 10 months of age) from wild-type mice, alpha-synuclein knockout mice, and alpha-synuclein BAC mice, which express human wild-type alpha-synuclein under all human regulatory elements in absence of mouse alpha-synuclein, providing human-like spatiotemporal expression of alpha-synuclein and recapitulating motor and pathological features of Parkinson’s disease. We identified specific changes in synaptic vesicle proteins that capture aging and synucleinopathies. These findings not only provide new insights into synaptic vesicle biology and mechanisms of synucleinopathy, but also offer a baseline for further mechanistic exploration of age- and disease-related alterations in synaptic vesicles.
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Project description:LUHMES cells share many characteritics with human dopamingeric neurons in the substantia nigra, the cells whose demise is responsible for the motor symptoms in Parkinson’s disease (PD). LUHMES cells can therefore be used bona fide as a model to study pathophysiological processes involved in PD. Previously, we showed that LUHMES cell degenerate after six days upon overexpression of wild type alpha-synuclein. In the present study we performed a transcriptome and proteome expression analysis in alpha-synuclein-overexpressing cells and GFP-expressing control cells in order to identify genes and proteins that are differentially regulated upon overexpression of alpha-synuclein. The analysis was performed four days after the initiation of alpha-synuclein or GFP overexpression, before the cells died in order to identify processes that preceded cell death.
2022-05-19 | PXD028322 | Pride
Project description:Here we explore the striatum transcriptomic effects of alpha-synuclein administration in mice as model of Parkinson´s disease. Moreover, we also explore the neuroprotective effect of cannabonoid-based druga (VCE-003.2) as a potential neuroportective agent in Parkinson´s disease
2024-11-30 | E-MTAB-13768 | biostudies-arrayexpress
Project description:Previous studies have demonstrated an importance of alpha-synuclein as a modulator of various mechanisms implicated in chemical neurotransmission but information about other two synuclein family members’ involvement in molecular processes taking place in presynaptic terminals is limited. Here we demonstrated that dopamine uptake by synaptic vesicles isolated from the striatum of mice lacking beta-synuclein was significantly reduced. Reciprocally, reintroduction, either in vivo or in vitro, of beta-synuclein but not alpha- or gamma-synuclein improved uptake by vesicles isolated from the striatum of triple alpha/beta/gamma-synuclein deficient mice. Proteomic analysis of synuclein-free and beta-synuclein-only-containing synaptic vesicles suggested that mechanistically, beta-synuclein potentiates vesicular monoamine transporter 2 (VMAT2)-dependent dopamine uptake by assembling specific multiprotein complexes comprised of resident vesicular proteins and transiently associated, predominantly cytosolic proteins. The increased availability of such complexes on the surface of striatal synaptic vesicles lacking other synucleins should also promote sequestration of 1-methyl-4-phenylpyridinium (MPP+), a toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which explains the resistance of dopaminergic neurons of substantia nigra lacking alpha-synuclein and/or gamma-synuclein to this neurotoxin.
2022-02-17 | PXD027786 | Pride
Project description:Microarray comparison of transgenic mice overexpressing human alpha-synuclein under the PDGF beta promoter to wildtype littermates at 3 months and 9 months of age. RNA was extracted from substantia nigral cells that were isolated by laser capture microdissection.
2007-12-20 | E-MEXP-1383 | biostudies-arrayexpress