Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

ABSTRACT: Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

PROVIDER: PRJNA340132 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR4064270_1.fastq.gz	Fastqsanger.gz
	SRR4064270_2.fastq.gz	Fastqsanger.gz
	SRR4064269_1.fastq.gz	Fastqsanger.gz
	SRR4064269_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray2]

Project description:Electromagnetic fields (EMF) are physical energy generated by electrically charged objects that can influence numerous biologic processes, including control of cell fate and plasticity. In this study, we show that magnetic gold nanoparticles in the presence of EMF can facilitate efficient direct lineage reprogramming to induced dopamine neurons both in vitro and in vivo. Remarkably, electromagnetic stimulation leads to the specific activation of the histone acetyl transferase Brd2, resulting in H3K27 acetylation and robust activation of neuronal-specific gene expression. In vivo reprogramming in conjunction with EMF stimulation efficiently alleviated symptoms in a mouse model of Parkinson’s disease (PD) in a noninvasive and controllable manner. These studies provide a proof of principle that EMF-based approaches may represent a viable and safe therapeutic strategy facilitating in vivo lineage conversion for neurodegenerative disorders.

2018-04-10 | GSE86051 | GEO

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [microarray1]

2018-04-10 | GSE86050 | GEO

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [ChIP-Seq]

2018-04-10 | GSE86049 | GEO

Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson's disease therapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-10 | GSE86052 | GEO

Mitochondrial proteomics investigation of a cellular model of impaired dopamine homeostasis, an early step in Parkinson's disease pathogenesis

Project description:Impaired dopamine homeostasis is an early event in the pathogenesis of Parkinson's disease. Generation of intracellular reactive oxygen species consequent to dopamine oxidation leads to mitochondrial dysfunction and eventually cell death. Alterations in the mitochondrial proteome due to dopamine exposure were investigated in the SH-SY5Y human neuroblastoma cell line. The combination of two orthogonal proteomic approaches, two-dimensional electrophoresis and shotgun proteomics, was used to highlight the specific pathways perturbed by the increase of intracellular dopamine, in comparison with those perturbed by a specific mitochondrial toxin (4-methyphenylpyridinium, MPP+), a neurotoxin causing Parkinsonism-like symptoms in animal models. Proteins altered by MPP+ did not completely overlap with those affected by dopamine treatment. In particular, the MPP+ target complex I component NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 was not affected by dopamine together with 26 other proteins. The comparison of proteomics approaches highlighted the fragmentation of some mitochondrial proteins, suggesting an alteration of the mitochondrial protease activity. Pathway and disease association analysis of the proteins affected by dopamine revealed the overrepresentation of the Parkinson's disease and the parkin-ubiquitin proteasomal system pathways and of gene ontologies associated to generation of precursor metabolites and energy, response to topologically incorrect proteins and programmed cell death. These alterations may be globally interpreted in part as the result of a direct effect of dopamine on mitochondria (e.g. alteration of the mitochondrial protease activity) and in part as the effect on mitochondria of a general activation of cellular processes (e.g. regulation of programmed cell death).

2014-04-15 | PXD000838 | Pride

Pulsed electromagnetic field therapy alters the genomic profile of bladder cancer cell line HT-1197

Project description:Bladder cancer cell lines were subjected to either pulsed electromagnetic field therapy (PEMF) or control (no PEMF) 1 hour/day for a total of 5 days to assess changes in genomic analysis.

2025-03-20 | GSE292216 | GEO

Amplitude Modulated Radiofrequency Electromagnetic Field Treatment Combined With TAS-102 (Lonsurf) in Refractory Metastatic Colorectal Cancer

Project description:Combined chemotherapy and radiofrequency electromagnetic field treatment for patients with liver dominant refractory metastatic colorectal cancer

| 69709 | ecrin-mdr-crc

Semi-quantitative proteomics of mammalian cells exposed to non-ionizing electromagnetic fields

Project description:Unbiased SILAC-based proteomics of human and mouse cells exposed to non-ionizing electromagnetic fields (EMFs) such as those emitted by power-lines (ELF), mobile cellular systems (UMTS) and wireless networking devices (WiFi).

2017-02-01 | PXD002862 | Pride

The dopamine transporter antiports potassium to increase the uptake of dopamine

Project description:The dopamine transporter facilitates dopamine reuptake from the extracellular space to terminate neurotransmission. The transporter belongs to the neurotransmitter:sodium symporter family, which includes transporters for serotonin, norepinephrine, and GABA that utilize the Na+ gradient to drive the uptake of substrate. Decades ago, it was shown that the serotonin transporter also antiports K+, but investigations of K+-coupled transport in other neurotransmitter:sodium symporters have been inconclusive. Here, we show that ligand binding to the drosophila- and human dopamine transporters are inhibited by K+, and the conformational dynamics of the drosophila dopamine transporter in K+ are divergent from the apo- and Na+-states. Furthermore, we found that K+ increased dopamine uptake by the drosophila dopamine transporter in liposomes, and visualized Na+ and K+ fluxes in single proteoliposomes using fluorescent ion indicators. Our results expand on the fundamentals of dopamine transport and prompt a reevaluation of the impact of K+ on other transporters in this pharmacologically important family.

2022-05-20 | PXD032663 | Pride

PT109B Rapidly Converts Astrocytes to Dopaminergic Neurons and Alleviates Parkinson's Disease in Mice.

Project description:Reprogramming astrocytes into neurons using chemical small molecules has emerged as a promising therapeutic strategy for Parkinson's disease (PD). Here, we have identified PT109B, a novel multi-kinase inhibitor, as a potent agent that induces the direct reprogramming of astrocytes into functional induced dopaminergic neurons (iDANs) beginning with a remarkably short 6-hour window. Within just half a month, PT109B facilitated the maturation of iDANs, characterized by synaptic structures, electrophysiological properties, sustained dopamine release, and long-term viability (for over 3 months). Mechanistically, PT109B drove this conversion through cell cycle arrest, astrocytic activation, and upregulation of key basic Helix-Loop-Helix (b-HLH) transcription factors, including NeuroD1, Nurr1, Ngn2, and Ascl1. Importantly, oral administration of PT109B in a 6-OHDA-induced PD mouse model exhibited significant therapeutic efficacy by reprogramming astrocytes to functional neurons in the striatum, leading to improved motor functions. These findings suggest PT109B as a promising therapeutic candidate for PD.

2026-01-01 | GSE292869 | 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