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Project description:The SH-SY5Y Human neuroblastoma cell line was subcloned from the SK-N-SH cell line, which has been isolated from a bone marrow biopsy of a 4 year-old female patient. To examine the transcriptional regulation by ERRα and ERRγ in human neuronal cells, we investigated chromatin binding regions of ERRαlpha and ERRγ genome-wide in the SH-SY5Y cells. We detected thier target genes, which were largely overlap.
2024-08-20 | GSE227296 | GEO
Project description:Genome-wide analysis of the transcriptional regulation by ERRα and ERRγ in SH-SY5Y cells
| PRJNA944596 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-03-09 | GSE149560 | GEO
Project description:Multiple genetic and environmental factors play a role in the development and progression of Parkinson's disease (PD). The main neuropathological hallmark of PD is the degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta. To study genetic and molecular contributors to the disease process, there is a great need for readily accessible cells with prominent DAergic features that can be used for reproducible in vitro cellular screening. Here, we investigated the molecular phenotype of retinoic acid (RA) differentiated SH-SY5Y cells using genome wide transcriptional profiling combined with gene ontology, transcription factor and molecular pathway analysis. We demonstrated that RA induces a general neuronal differentiation program in SH-SY5Y cells and that these cells develop a predominantly mature DAergic-like neurotransmitter phenotype. This phenotype is characterized by increased dopamine levels together with a substantial suppression of other neurotransmitter phenotypes, such as those for noradrenaline, acetylcholine, glutamate, serotonin and histamine. In addition, we show that RA differentiated SH-SY5Y cells express the dopamine and noradrenalin neurotransmitter transporters that are responsible for uptake of MPP(+), a well known DAergic cell toxicant. MPP(+) treatment alters mitochondrial activity according to its proposed cytotoxic effect in DAergic neurons. Taken together, RA differentiated SH-SY5Y cells have a DAergic-like phenotype, and provide a good cellular screening tool to find novel genes or compounds that affect cytotoxic processes that are associated with PD.
| S-EPMC3665836 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-12-01 | GSE94485 | GEO
Project description:BackgroundDown syndrome (DS) is characterized by a genome-wide profile of differential DNA methylation that is skewed towards hypermethylation in most tissues, including brain, and includes pan-tissue differential methylation. The molecular mechanisms involve the overexpression of genes related to DNA methylation on chromosome 21. Here, we stably overexpressed the chromosome 21 gene DNA methyltransferase 3L (DNMT3L) in the human SH-SY5Y neuroblastoma cell line and assayed DNA methylation at over 26 million CpGs by whole genome bisulfite sequencing (WGBS) at three different developmental phases (undifferentiated, differentiating, and differentiated).ResultsDNMT3L overexpression resulted in global CpG and CpG island hypermethylation as well as thousands of differentially methylated regions (DMRs). The DNMT3L DMRs were skewed towards hypermethylation and mapped to genes involved in neurodevelopment, cellular signaling, and gene regulation. Consensus DNMT3L DMRs showed that cell lines clustered by genotype and then differentiation phase, demonstrating sets of common genes affected across neuronal differentiation. The hypermethylated DNMT3L DMRs from all pairwise comparisons were enriched for regions of bivalent chromatin marked by H3K4me3 as well as differentially methylated sites from previous DS studies of diverse tissues. In contrast, the hypomethylated DNMT3L DMRs from all pairwise comparisons displayed a tissue-specific profile enriched for regions of heterochromatin marked by H3K9me3 during embryonic development.ConclusionsTaken together, these results support a mechanism whereby regions of bivalent chromatin that lose H3K4me3 during neuronal differentiation are targeted by excess DNMT3L and become hypermethylated. Overall, these findings demonstrate that DNMT3L overexpression during neurodevelopment recreates a facet of the genome-wide DS DNA methylation signature by targeting known genes and gene clusters that display pan-tissue differential methylation in DS.
| S-EPMC7942011 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-11-05 | GSE212754 | GEO
Project description:ObjectiveAlzheimer's disease (AD) is one of the major disorders worldwide. Recent research suggests that the amyloid-? precursor protein intracellular domain (AICD) is a potential contributor to AD development and progression. The small AICD is rapidly degraded after processing from the full-length protein. The present study aimed to apply a highly efficient biotinylation approach in vitro to study AICD-associated complexes in neurocytes.MethodsBy co-expressing Escherichia coli biotin ligase with biotinyl-tagged AICD in the SH-SY5Y neuronal cell line, the effects of AICD overexpression on cell proliferation and apoptosis were analyzed. Besides, AICD-associated nuclear transcriptional complexes were purified and then examined by mass spectrometry.ResultsOur data showed that AICD overexpression not only affected cell proliferation but also led to apoptosis in differentiated SH-SY5Y cells. Moreover, biotinylation allowed single-step purification of biotinylated AICD-associated complexes from total nuclear extract via high-affinity biotin-streptavidin binding. Following this by mass spectrometry, we identified physically associated proteins, some reported previously and other novel binding partners, CUX1 and SPT5.ConclusionBased on these results, a map of the AICD-associated nuclear interactome was depicted. Specifically, AICD can activate CUX1 transcriptional activity, which may be associated with AICD-dependent neuronal cell death. This work helps to understand the AICD-associated biological events in AD progression and provides novel insights into the development of AD.
| S-EPMC5560331 | biostudies-literature
Project description:Toxoplasma rhoptry protein 16 (ROP16) is crucial in the host-pathogen interaction by acting as a virulent factor during invasion. To improve understanding of the molecular function underlying the effect of ROP16 on host cells, the present study analyzed the transcriptional profile of genes in the ROP16‑transfected SH‑SY5Y human neuroblastoma cell line. The transcriptional profile of the SH‑SY5Y human neuroblastoma cell line overexpressing ROP16 were determined by microarray analysis in order to determine the host neural cell response to the virulent factor. Functional analysis was performed using the Protein Analysis Through Evolutionary Relationships classification system. The ToppGene Suite was used to select candidate genes from the differentially expressed genes. A protein‑protein interaction network was constructed using Cytoscape software according to the interaction associations determined using the Search Tool for the Retrieval of Interacting Genes/Proteins. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis of the selected genes confirmed the results of the microarray. The results showed that 383 genes were differentially expressed in response to ROP16 transfection, of which 138 genes were upregulated and 245 genes were downregulated. Functional analysis indicated that the differentially expressed genes (DEGs) were involved in several biological processes, including developmental process, biological regulation and apoptotic process. A total of 15 candidate genes from the DEGs were screened using the ToppGene Suite. No significant differences in expression were observed between the RT‑qPCR data and the microarray data. Transfection with ROP16 resulted in alterations of several biological processes, including nervous system development, apoptosis and transcriptional regulation. Several genes, including CXCL12, BAI1, ZIC2, RBMX, RASSF6, MAGE‑A6 and HOX, were identified as significant DEGs. Taken together, these results may contribute to understanding the mechanisms underlying the functions of ROP16 and provide scope for further investigation of the pathogenesis of Toxoplasma gondii.
| S-EPMC5101894 | biostudies-literature
Project description:STIM1 is an endoplasmic reticulum (ER) protein that modulates the activity of a number of Ca2+ transport systems. By direct physical interaction with ORAI1, a plasma membrane Ca2+ channel, STIM1 activates the ICRAC current, whereas the binding with the voltage-operated Ca2+ channel CaV1.2 inhibits the current through this latter channel. In this way, STIM1 is a key regulator of Ca2+ signaling in excitable and non-excitable cells, and altered STIM1 levels have been reported to underlie several pathologies, including immunodeficiency, neurodegenerative diseases, and cancer. In both sporadic and familial Alzheimer's disease, a decrease of STIM1 protein levels accounts for the alteration of Ca2+ handling that compromises neuronal cell viability. Using SH-SY5Y cells edited by CRISPR/Cas9 to knockout STIM1 gene expression, this work evaluated the molecular mechanisms underlying the cell death triggered by the deficiency of STIM1, demonstrating that STIM1 is a positive regulator of ITPR3 gene expression. ITPR3 (or IP3R3) is a Ca2+ channel enriched at ER-mitochondria contact sites where it provides Ca2+ for transport into the mitochondria. Thus, STIM1 deficiency leads to a strong reduction of ITPR3 transcript and ITPR3 protein levels, a consequent decrease of the mitochondria free Ca2+ concentration ([Ca2+]mit), reduction of mitochondrial oxygen consumption rate, and decrease in ATP synthesis rate. All these values were normalized by ectopic expression of ITPR3 in STIM1-KO cells, providing strong evidence for a new mode of regulation of [Ca2+]mit mediated by the STIM1-ITPR3 axis.
| S-EPMC7555297 | biostudies-literature