Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of cytochrome c in α-synuclein radical formation: implications of α-synuclein in neuronal death in Maneb and paraquat-induced model of Parkinson's disease

ABSTRACT: Altogether results show that peroxidase activity of cytochrome c contributes to α-synuclein radical formation and oligomerization, and that α-synuclein through its co-localization with cytochrome c or on it's own, affects several biological pathways which contribute to increased neuronal death in Maneb and paraquat (MP)-induced model of Parkinson's disease.

ORGANISM(S): Mus musculus

PROVIDER: GSE89562 | GEO | 2016/11/29

SECONDARY ACCESSION(S): PRJNA352558

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-Sequencing from ventral mid brain and striatum of paraquat, pyridaben and paraquat+maneb mice models of Parkinson's disease.

Project description:We report RNA-sequencing from ventral mid brain and striatum from paraquat, pyridaben and paraquat+maneb mice models of Parkinson's disease. We observed several differentially expressed genes upon pesticide exposure which we analyzed by pathway analysis.

2012-09-04 | GSE36232 | GEO

RNA-Sequencing from ventral mid brain and striatum of paraquat, pyridaben and paraquat+maneb mice models of Parkinson's disease.

2012-09-04 | E-GEOD-36232 | biostudies-arrayexpress

Gene expression of A53T and corrected IPSC driven to DA neurons and exposed to paraquat and maneb

Project description:Parkinson disease (PD) is characterized by extensive loss of A9 dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). A strong association has been reported between PD and exposure to mitochondrial toxins such as the environmental pesticides paraquat, maneb, and rotenone. Here, using a robust, patient-derived, stem cell model of PD that allows comparison of -synuclein ( -syn) mutant cells and isogeneic mutation-corrected controls, we identify mitochondrial toxin-induced perturbations specific to A53T -syn mutant A9-DA neurons (hNs). We report a novel molecular pathway whereby basal as well as toxin-induced oxidative and nitrosative stress inhibits the MEF2C-PGC1 transcription network in A53T hNs compared to corrected controls, contributing to mitochondrial dysfunction and apoptotic cell death. Our data provide mechanistic insight into gene-environmental interaction (GxE) in the pathogenesis of PD. Furthermore, using small molecule high-throughput screening, we identify the MEF2C-PGC1 pathway as a new drug target for therapeutic benefit in PD. In the current study, isogenic hiPSCs differing exclusively at a single amino acid (A53T) were exposed to either 2.8uM paraquat in combination with 1uM maneb for 24h or PBS vehicle control. Gene expression profile was analysed to assess the effect of both the genotype and exposure regiment on gene expression.

2013-12-05 | E-GEOD-46798 | biostudies-arrayexpress

α-Synuclein promotes H4R3me2s through interacting with BAF-PRMT5 complex

Project description:We conducted a screening for nuclear proteins which interact with α-synuclein by mass-spectrometry. As a result, we found that α-synuclein interact with BAF complex. Furthermore, overexpressed α-synuclein increased global H4R3me2s by promoting interaction between BAF complex and PRMT5 in cultered cells. In this study, we explored the influence of overexpressed α-synuclein on H4R3me2s by ChIP-seq using anti-H4R3me2s antibody.

2023-11-23 | GSE228331 | GEO

Alpha-synuclein deficiency affects brain Foxp1 expression and ultrasonic vocalization

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

Mus musculus

Project description:Role of cytochrome c in α-synuclein radical formation: implications of α-synuclein in neuronal death in Maneb and paraquat-induced model of Parkinson's disease

| PRJNA352558 | ENA

Dietary intake of α-ketoglutarate ameliorates α-synuclein pathology in a Parkinson’s disease mouse model

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).

2022-10-02 | GSE214446 | GEO

Glial and neuronal alpha synuclein induce unique transcriptional programs

Project description:We performed RNAseq using whole Drosophila heads after expressing human wild type alpha synuclein in either glia, neurons, or both types. We identified many upregulated genes when alpha synuclein was expresed in glia and many downregulated genes with it was expresed in neurons or both cell types.

2019-09-30 | GSE128120 | GEO

Phenotypic manifestation of alpha-synuclein strains from Parkinson’s disease and multiple system atrophy in human dopaminergic neruons

Project description:Although α-synucleinis implicated in the pathogenesis of Parkinson’s disease and related disorders, it remains unclear whether specific conformations or levels of α-synuclein assemblies are toxic and how they cause progressive loss of human dopaminergic neurons. To address this issue, we used iPSC-derived dopaminergic neurons with a-synuclein triplication or controls where endogenous α-synuclein was imprinted into synthetic or disease-relevant conformations. We used α-synuclein fibrils generated de novo or amplified from homogenates of brains affected with Parkinson’s disease (n=3) .We found that a 2.5-fold increase in α-synuclein levels in α-synuclein gene triplication neurons promoted seeded aggregation in a dose and time-dependent fashion, which was associated with a further increase in α-synuclein gene expression.Transcriptomic analysis and isogenic correction of α-synuclein triplication revealed that intraneuronal α-synuclein levels solely and sufficiently explained vulnerability to cell death.

2020-09-02 | GSE149632 | GEO

RNA Bind-N-Seq for purified α-Synuclein and BG4 (scFV for G-quadruplex)

Project description:Aggregation of α-synuclein may trigger the development of synucleinopathies, a progressive neurodegenerative disease such as Parkinson's disease and Dementia with Lewy bodies. We demonstrate RNA initiates α-synuclein phase transition in vitro, however, RNA binding ability and its motif remain unclear. Here, we indicate purified human α-synuclein protein preferentially binds to guanine-rich RNA sequences by RNA Bind-N-Seq using a pool of random 24-mer RNA oligonucleotides in vitro. Importantly, these hit motifs were required consecutive guanines not random, suggesting that RNA G-quadruplexes binds to α-synuclein. We also confirmed that GC content and skew of α-synuclein-enriched RNA sequences were similar to that of BG4 (G-quadruplex antibody)-enriched RNA sequences. Taken together, these data suggest that α-synuclein binds to RNA-formed G-quadruplex.

2023-07-17 | GSE235418 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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