PGC-1a overexpression in SH-SY5Y cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA636085 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11881233_1.fastq.gz | Fastqsanger.gz | |||
| SRR11881233_2.fastq.gz | Fastqsanger.gz | |||
| SRR11881234_1.fastq.gz | Fastqsanger.gz | |||
| SRR11881234_2.fastq.gz | Fastqsanger.gz | |||
| SRR11881235_1.fastq.gz | Fastqsanger.gz |
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Project description:SH-SY5Y cells were transfected with either GFP control or PGC-1a overexpression adenovirus and RNA was isolated after 48 hours and sequenced in order to understand what genes are differentially expressed with the presence of PGC-1a in neuron like cells. This experiment shows that genes related to neuron health and mitochondiral function are controlled by PGC-1a. We also analyze the promoter of upregualted genes found here to figure out potential partners that co-regulate with PGC-1a.
2021-05-31 | GSE151499 | GEO
Project description:The aim of this experiment is to study the gene expression response of DLG2 overexpression in neuroblastoma. Four different conditions were compared in neuroblastoma SH-SY5Y cells, with 4 biological replicates each: 1) Control (no DLG2 overexpression, no retinoic acid treatment), 2) RA (no DLG2 overexpression, retinoic acid treatment), 3) DLG2 (DLG2 overexpression, no retinoic acid treatment), 4) DLG2-RA (DLG2 overexpression, retinoic acid treatment)
2020-08-13 | E-MTAB-8657 | biostudies-arrayexpress
Project description:RNA-Seq of SH-SY5Y cells after DLG2 overexpression
| PRJEB36186 | ENA
Project description:The peroxisome proliferator-activated receptor c coactivator 1 (PGC-1) proteins are key regulators of cellular bioenergetics and are accordingly expressed in tissues with a high energetic demand. For example, PGC-1a and PGC-1b control organ function of brown adipose tissue, heart, brain, liver and skeletal muscle. Surprisingly, despite their prominent role in the control of mitochondrial biogenesis and oxidative metabolism, expression and function of the PGC-1 coactivators in the retina, an organ with one of the highest energy demands per tissue weight, are completely unknown. Moreover, the molecular mechanisms that coordinate energy production with repair processes in the damaged retina remain enigmatic. In the present study, we thus investigated the expression and function of the PGC-1 coactivators in the healthy and the damaged retina. We show that PGC-1a and PGC-1b are found at high levels in different structures of the mouse retina, most prominently in the photoreceptors. Furthermore, PGC-1a knockout mice suffer from a striking deterioration in retinal morphology and function upon detrimental light exposure. Gene expression studies revealed dysregulation of all major pathways involved in retinal damage and apoptosis, repair and renewal in the PGC-1a knockouts. The light-induced increase in apoptosis in vivo in the absence of PGC-1a was substantiated in vitro, where overexpression of PGC-1a evoked strong anti-apoptotic effects. Finally, we found that retinal levels of PGC-1 expression are reduced in different mouse models for retinitis pigmentosa. We demonstrate that PGC-1a is a central coordinator of energy production and, importantly, all of the major processes involved in retinal damage and subsequent repair. Together with the observed dysregulation of PGC-1a and PGC-1b in retinitis pigmentosa mouse models, these findings thus imply that PGC-1a might be an attractive target for therapeutic approaches aimed at retinal degeneration diseases.
2016-04-15 | GSE80265 | GEO
Project description:Huntington’s Disease (HD) is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin protein. Transcriptional deregulation and altered energy metabolism have been implicated in HD pathogenesis. We report here that mutant huntingtin causes disruption of mitochondrial function by inhibiting expression of PGC-1a, a transcriptional coactivator that regulates several metabolic processes including mitochondrial biogenesis and respiration. Mutant huntingtin represses PGC-1a gene transcription by associating with the promoter and interfering with the CREB/TAF4-dependent transcriptional pathway critical for the regulation of PGC-1a gene expression. Crossbreeding of PGC-1a knockout mice with HD knock-in mice leads to increased neurodegeneration of striatal neurons and motor abnormalities in the HD mice. Importantly, expression of PGC-1a partially reverses the toxic effects of mutant huntingtin in cultured striatal neurons. Moreover, lentiviral-mediated delivery of PGC-1a in the striatum provides neuroprotection in the transgenic HD mice. These studies suggest a key role for PGC-1a in the control of energy metabolism in the early stages of HD pathogenesis. Keywords: PGC-1a, striatum
2006-10-05 | GSE5786 | GEO
Project description:PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator-1alpha) coactivators regulate adaptive gene expression in response to challenges such as cold exposure, fasting, or physical exercise to balance energy supply and demand. Transcription of a single PGC-1α gene produces different isoforms (e.g. PGC-1α1 to α4) with different biological functions. We aimed to characterize the nuclear interactome for each PGC-1α variant, in particular the transcription factors they bind to regulate gene expression. This was done by generating GST-fusions of all PGC-1a variants, expressed in an insect cell system. These were used to capture associated protein complexes from HeLa nuclear extracts.
2022-03-01 | PXD009232 | Pride
Project description:Investigation of whole genome gene expression level changes in SH-SY5Y cells transfected Pea3-VP16 cells compared to pCDNA3 transfected cells as a control.
2017-01-11 | E-MTAB-5324 | biostudies-arrayexpress
Project description:Investigation of whole genome expression in SH-SY5Y cells transfected Elk-1-VP16 cells compared to pCDNA3 transfected cells as a control.
2021-02-28 | E-MTAB-9938 | biostudies-arrayexpress
Project description:Background: SH-SY5Y cells exhibit a neuronal phenotype when treated with all-trans retinoic acid (RA), but the molecular mechanism of activation in the signaling pathway mediated by phosphatidylinositol 3-kinase (PI3K) is not sufficiently understood. To shed new light on the mechanism, we comprehensively compared the gene expression profiles between SK-N-SH cells and two subtypes of SH-SY5Y cells (SH-SY5Y-A and SH-SY5Y-E), each of which showed a different phenotype during RA-mediated differentiation. Results: SH-SY5Y-A cells differentiated in the presence of RA, whereas RA-treated SH-SY5Y-E cells required additional treatment with brain-derived neurotrophic factor (BDNF) for full differentiation. In combination with perturbation using a PI3K inhibitor, LY294002, we identified 386 genes and categorized them into two clusters dependent on the PI3K signaling pathway during RA-mediated differentiation in SH-SY5Y-A cells. Transcriptional regulation of the gene cluster was greatly reduced in SK-N-SH cells or partially impaired in SH-SY5Y-E cells in coincidence with a defect in the neuronal phenotype of these cell lines. Additional stimulation with BDNF induced a set of neural genes which were down-regulated in RA-treated SH-SY5Y-E cells but were abundant in the differentiated SH-SY5Y-A cells. Conclusions: We identified the gene clusters controlled by PI3K- and TRKB-mediated signaling pathways during differentiation in two subtypes of SH-SY5Y cells. TRKB-mediated bypass pathway compensates for the impaired neural functions generated by defects in several signaling pathways including PI3K in SH-SY5Y-E cells. The expression profiling data are useful for further studies to elucidate the signal transduction-transcriptional network including PI3K and/or TRKB. Keywords: Cell type comparison, time course
2009-09-01 | GSE9169 | GEO
Project description:Human SH-SY5Y neuroblastoma cells treated with paraquat, a neurotoxic herbicide which both catalyzes the formation of reactive oxygen species (ROS) and induces mitochondrial damage in animal models was profiled using Affimetrix Exon 1.0 ST GeneChips® Human SH-SY5Y neuroblastoma cells was compared with respect to Human SH-SY5Y neuroblastoma cells treated with Paraquat. Parqaut treatment was done as described by Maracchioni, A., Totaro, A., Angelini, D.F., Di Penta, A., Bernardi, G., Carri, M.T., and Achsel, T. (2007) J Neurochem 100, 142-153
2010-12-22 | E-GEOD-21305 | biostudies-arrayexpress