Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14475437_1.fastq.gz | Fastqsanger.gz | |||
| SRR14475437_2.fastq.gz | Fastqsanger.gz | |||
| SRR14475438_1.fastq.gz | Fastqsanger.gz | |||
| SRR14475438_2.fastq.gz | Fastqsanger.gz | |||
| SRR14475439_1.fastq.gz | Fastqsanger.gz |
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Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.
2022-05-10 | GSE174121 | GEO
Project description:GPR17 silencing in OPCs accelerates their differentiation into fully mature oligodendrocytes. We performed a whole microarray profiling to identify altered signaling pathways after GPR17 silencing that are responsible for its effect on oligodendrocyte maturation.
2022-08-03 | GSE208409 | GEO
Project description:Hypothalamic neurons expressing Agouti-related peptide (AgRP) are critical for initiating food intake, but druggable biochemical pathways that control this response remain elusive. Thus, genetic ablation of insulin or leptin signaling in AgRP neurons is predicted to reduce satiety but fails to do so. FoxO1 is a shared mediator of both pathways, and its inhibition is required to induce satiety. Accordingly, FoxO1 ablation in AgRP neurons of mice results in reduced food intake, leanness, improved glucose homeostasis, and increased sensitivity to insulin and leptin. Expression profiling of flow-sorted FoxO1-deficient AgRP neurons identifies G-protein-coupled receptor Gpr17 as a FoxO1 target whose expression is regulated by nutritional status. Intracerebroventricular injection of Gpr17 agonists induces food intake, whereas Gpr17 antagonist cangrelor curtails it. These effects are absent in Agrp-Foxo1 knockouts, suggesting that pharmacological modulation of this pathway has therapeutic potential to treat obesity. We used microarrays to detail the change of gene expression in AgRP neurons after knocking out FoxO1. AgRP neurons from control and KO mice were collected by FACS. Gene expression was analyzed by microarray.
2013-04-09 | E-GEOD-45858 | biostudies-arrayexpress
Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.
2022-05-10 | GSE174122 | GEO
Project description:Hypothalamic neurons expressing Agouti-related peptide (AgRP) are critical for initiating food intake, but druggable biochemical pathways that control this response remain elusive. Thus, genetic ablation of insulin or leptin signaling in AgRP neurons is predicted to reduce satiety but fails to do so. FoxO1 is a shared mediator of both pathways, and its inhibition is required to induce satiety. Accordingly, FoxO1 ablation in AgRP neurons of mice results in reduced food intake, leanness, improved glucose homeostasis, and increased sensitivity to insulin and leptin. Expression profiling of flow-sorted FoxO1-deficient AgRP neurons identifies G-protein-coupled receptor Gpr17 as a FoxO1 target whose expression is regulated by nutritional status. Intracerebroventricular injection of Gpr17 agonists induces food intake, whereas Gpr17 antagonist cangrelor curtails it. These effects are absent in Agrp-Foxo1 knockouts, suggesting that pharmacological modulation of this pathway has therapeutic potential to treat obesity. We used microarrays to detail the change of gene expression in AgRP neurons after knocking out FoxO1.
2013-04-09 | GSE45858 | GEO
Project description:Chronic neuroinflammation disrupts oligodendrocyte differentiation and limits effective remyelination across multiple neurological disorders. Among the molecular regulators integrating inflammatory cues with oligodendrocyte maturation, G protein-coupled receptor 17 (GPR17) has emerged as a critical checkpoint. Physiologically, GPR17 expression is low in early oligodendrocyte precursors (OPCs) and peaks in immature oligodendrocytes, after which it must be downregulated to allow cells’ terminal maturation. Under neuroinflammatory conditions, GPR17 is permanently upregulated, suggesting a role in blockade of oligodendrocyte (OL) maturation and in defective myelination. Here, we tested whether receptor modulation by the specific agonist Galinex (GAL) can restore proper OL maturation under neuroinflammatory conditions. We first showed that subtoxic inflammatory stress, defined as cytokine exposure that did not cause overt loss of cell viability, consistently impaired oligodendrocyte morphological maturation, reduced the expression of myelin-associated markers, and was accompanied by increased GPR17 expression. Transcriptomics analysis revealed that CTK (Cytokines) induced coordinated transcriptional remodelling involving protein synthesis/proteostasis, mitochondrial metabolism, and lipid-related pathways, together with a shift towards an immunogenic-like, senescence/DNA-damage–associated phenotype. Cross-comparison with publicly available transcriptomic signatures of neuroinflammatory patterns from both mouse models and Alzheimer’s and multiple sclerosis human brains, revealed significant overlap with disease-associated modules, supporting the relevance of the inflammatory pathways engaged in our model. We then showed that treatment of OLs with GAL restored cells’ terminal maturation and morphological features. Moreover, in a synthetic nanofiber myelination assay, GAL significantly increased the length of myelinated segments compared to CTK-treated cells, suggesting an improvement of OL myelinating capacity after inflammatory damage. Together, this study establishes a controlled in vitro model linking alteration of disease-relevant transcriptional pathways to impaired OL differentiation and highlights GPR17 pharmacological modulation as a feasible strategy to promote OL maturation under non permissive inflammatory contexts.
2026-06-25 | GSE331058 | GEO
Project description:ZBTB7B Inhibits Glioma Tumorigenicity by Upregulating GPR17 and CXCL10
| PRJNA1227451 | ENA
Project description:Gene expression analysis after GPR17 silencing in oligodendrocyte precursor cells (OPCs)
| PRJNA859818 | ENA
Project description:Background: We utilized a CRISPR-Cas9 screening library to examine the functions of tumor-related genes. Among these, we identified the transcription factor ZBTB7B, which overexpressed in breast cancer cells and significantly inhibited breast cancer growth in the brains of nude mice. Based on this finding, we hypothesized that ZBTB7B might exert similar effects on glioma, a possibility not yet explored in the literature. This study aims to evaluate the effects and mechanisms of ZBTB7B in glioma progression. Methods:The U118 and the GL261 cell line , both overexpressing ZBTB7B, were generated via lentiviral transduction. The impact of ZBTB7B on glioma growth was assessed using in vitro cell culture and in vivo intracranial inoculation. Downstream targets regulated by ZBTB7B were identified through transcriptome sequencing, PCR arrays, ELLA assays, and Western blotting. Cell apoptosis and the cell cycle were analyzed via flow cytometry. Multicolor immunofluorescence staining was performed to evaluate the expression and localization of ZBTB7B in human and mouse glioma tissues. Findings:Overexpression of ZBTB7B significantly inhibited glioma cell survival both in vitro and in vivo. Mechanistically, ZBTB7B upregulated the expression of GPR17, which suppressed PKA phosphorylation, promoted the generation of reactive oxygen species, and ultimately induced apoptosis. Additionally, ZBTB7B regulated the chemokine CXCL10, facilitating the recruitment of CD4+ and CD8+ T cells to the tumor periphery. Human glioma tissue microarray analysis revealed ZBTB7B expression was significantly reduced or absent in grade II to IV glioma samples. Interpretation:ZBTB7B exhibits significant tumor-suppressive effects and holds promise as a potential molecular target for glioma therapy.
2026-03-01 | GSE290306 | GEO
Project description:Next Generation Sequencing Facilitates Quantitative Analysis of U87-PLV03 and U87-GPR17 Transcriptomes
| PRJNA728459 | ENA