Homo sapiens strain:SH-SY5Y
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB19649 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Synuclein pathology effect on Mitochondrial DNA mutations
| PRJEB82845 | ENA
Project description:The goal of this study is to compare NGS-derived transcriptome profiling (RNA-seq) of alpha-synuclein expressing Sh-SY5Y cells vs. lacZ control protein and find characteristic changes that may be related to alpha-synucleinopathies. Our results showed the enrichments of p53 pathways, DNA damage responses, and cellular senescence. Further studies validated genes involved in such pathways.
2022-03-09 | GSE149559 | GEO
Project description:SPO11-promoted DNA double-strand breaks (DSBs) formation is a crucial step for meiotic recombination, and it is indispensable to detect the broken DNA ends accurately for dissecting the molecular mechanisms behind. Here, we report a novel technique, named DEtail-seq (DNA End tailing followed by sequencing), that can directly and quantitatively capture the meiotic DSB 3’ overhang hotspots at single-nucleotide resolution.
2023-01-08 | GSE154227 | GEO
Project description:Parkinson’s disease (PD) is a progressive neurodegenerative disorder lacking disease-modifying therapies. Brain cholesterol dysregulation constitutes a recognized pathogenic mechanism, yet therapeutic inhibition of cholesterol synthesis has proven ineffective or detrimental. Here, we identify ATP-binding cassette transporter A1 (ABCA1) as a pivotal regulator of brain cholesterol homeostasis in PD. Dysregulated cholesterol metabolism and elevated ABCA1 expression occur in the substantia nigra of post-mortem PD patients and established PD models. Crucially, normal human brain tissue exhibits high basal ABCA1 expression in PD-vulnerable regions, underscoring its physiological relevance. Single-cell transcriptomics reveals predominant Abca1 expression in murine substantia nigra astrocytes and dopaminergic neurons. We establish that PD-associated hyperactivity of astrocytic ABCA1 drives excessive cholesterol efflux, inducing neuronal cholesterol overload and injury. This overload amplifies ABCA1 specifically within neuronal lysosomes, facilitating pathological cholesterol import. Subsequent lysosomal cholesterol accumulation activates GPR155 signaling to initiate mTOR-mediated autophagy suppression, culminating in α-Synuclein aggregation and neurodegeneration. Conditional knockdown of Abca1 in dopaminergic neurons mitigates α-Synuclein pathology and neurodegeneration in vivo. Furthermore, molecular docking identifies magnesium citrate, an FDA-approved laxative, as a potent ABCA1 inhibitor. Magnesium citrate administration enhances dopaminergic neuronal survival dose-dependently in PD mice. Collectively, our findings delineate a novel ABCA1-regulated pathway driving PD pathogenesis, providing compelling genetic and pharmacological proof-of-concept supporting ABCA1 inhibition as a promising disease-modifying strategy for PD.
2026-08-27 | GSE303508 | GEO
Project description:Homo sapiens epigenomics project
| PRJDA62881 | ENA
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:Homo sapiens isolate:SH-SY5Y Raw sequence reads
| PRJNA1175680 | ENA
Project description:Homo sapiens isolate:SH-SY5Y Raw sequence reads
| PRJNA1483870 | ENA
Project description:Profiling the Evolution of Neuroprotection from Small Molecule Precursors to Functional Dipeptide Conjugates in SH-SY5Y cells
| PRJNA1463050 | ENA