Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1203971 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31845300_1.fastq.gz | Fastqsanger.gz | |||
| SRR31845300_2.fastq.gz | Fastqsanger.gz | |||
| SRR31845291_1.fastq.gz | Fastqsanger.gz | |||
| SRR31845291_2.fastq.gz | Fastqsanger.gz | |||
| SRR31845292_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 20 |
Similar Datasets
Project description:We report an upregulation of miR-16 in Paget's disease of bone which is to target the SQSTM1. When miR-16 is lost in Paget's disease, there is malignant transformation.
2017-04-18 | GSE87018 | GEO
Project description:We extracted total RNA from fingerstick samples of normal, chondrosarcoma and Paget's disease patients. We then constructed small RNA libraries using HD adapters in order to identify small RNA biomarkers
2021-08-13 | GSE87054 | GEO
Project description:Glioma associated Macrophages (GAMs) are the most abundant immune cell type within diffuse gliomas and their density correlates with poorer prognosis. GAMs consist of resident microglia and bone marrow derived (BDM) cells and increased BDM infiltration is thought to be associated with disease progression however no definitive human marker of BDM exists. This is particularly true of LGGs, In this study we perform multicompartmental sampling and analyse GAMs from the perspective of gene regulatory networks. We show that GAMs and BDMs consist of distinct GRNs driven by the same master transcription factor SPI1, and that an increased activation of the blood derived SPI1 signature is associated with poorer prognosis in LGGs. Defining GAMs in terms of GRNs instead of marker genes alone permits a better understanding of the transcirptional programs that drive disease progression in diffuse gliomas.
2023-06-30 | E-MTAB-12528 | biostudies-arrayexpress
Project description:Glioblastoma (GBM) remains an untreatable disease. Understanding of GBM’s infiltrative biology at the resection margin is limited, despite causing disease recurrence and progression. To address this, we generated a high-throughput single-nucleus (sn)RNA-seq and snATAC-seq multi-omic dataset from six tumors with distinct genomic drivers and combined it with spatial transcriptomics to characterize the unique molecular phenotype of GBM near the margin. By contrasting GBM-specific biology in matching “Core” vs. “Margin” dissections, we define unique, shared “GBM infiltration” and chromatin accessibility signatures near the margin. We prioritize EGFR as a top differentially expressed and accessible “Margin” marker across GBM subtypes, show its dynamic expression along a core-to-margin infiltration trajectory, and validate its role in migration through CRISPR/Cas9 deletion in two patient-derived models. ChIP-seq studies furthermore corroborate preferential TEAD1 binding at EGFR’s accessible regulatory elements. This validated multi-omic dataset enables further studies into tumor and microenvironment biology in the context of residual GBM disease.
2025-07-14 | GSE286415 | GEO
Project description:Rasmussen encephalitis is a unilateral encephalitis characterized by treatment-resistant epilepsy and progressive cognitive and motor decline. MRI reveals inflammation and neuropathology reveals reactive astrocytes, microglial activation, microglial nodules, T cell infiltration, and neuronal loss.
Despite the abundant evidence of altered signaling pathways in Rasmussen brain tissue and associated genetic variants, the mechanisms remain poorly understood, and it is uncertain which are a part or result of the underlying cause
In Rasmussen brain tissue, we identified by RNAseq altered immune signaling pathways, immune cell type annotation enrichment, and by whole exome sequencing HLA variants more common to Rasmussen. These findings demonstrate immune cell infiltration associated with innate and adaptive immune responses, as well as HLA variants that may increase vulnerability to RE.
2022-04-05 | MSV000089203 | MassIVE
Project description:Background: Physical exercise is beneficial to keep physical and mental health. The molecular mechanisms underlying exercise are still worth exploring. Methods: The healthy adult mice after six weeks of moderate-intensity exercise (experimental group) and sedentary mice (control group) were used to perform transcriptomic, proteomic, lactylation modification, and metabolomics analysis. In addition, gene sets related to hypoxia, glycolysis, and fatty acid metabolism were used to aid in the screening of hub genes. The mMCP-counter was employed to evaluate infiltration of immune cells in murine liver tissues. Results: Transcriptomics analysis revealed 82 intersection genes related to hypoxia, glycolysis, and fatty acid metabolism. Proteomics and lactylation modification analysis identified 577 proteins and 141 differentially lactylation modification proteins. By overlapping 82 intersection genes with 577 differentially expressed proteins and 141 differentially lactylation modification proteins, three hub genes (Aldoa, Acsl1, and Hadhb) were obtained. The immune infiltration analysis revealed a decreased score for monocytes/macrophages and an increased score for endothelial cells in the experimental group. Then, 459 metabolites in positive mode and 181 metabolites in negative mode were identified. The “Metabolic pathways” (mmu01100) was a common pathway between intersection genes-enriched pathways and metabolites-enriched pathways. Conclusion: These findings highlight the pivotal roles of hub genes in the glycolysis and fatty acid metabolism under the context of chronic exercise.
2025-02-10 | PXD057080 | Pride
Project description:Glioblastoma (GBM) remains an untreatable disease. Understanding of GBM’s infiltrative biology at the resection margin is limited, despite causing disease recurrence and progression. To address this, we generated a high-throughput single-nucleus (sn)RNA-seq and snATAC-seq multi-omic dataset from six tumors with distinct genomic drivers and combined it with spatial transcriptomics to characterize the unique molecular phenotype of GBM near the margin. By contrasting GBM-specific biology in matching “Core” vs. “Margin” dissections, we define unique, shared “GBM infiltration” and chromatin accessibility signatures near the margin. We prioritize EGFR as a top differentially expressed and accessible “Margin” marker across GBM subtypes, show its dynamic expression along a core-to-margin infiltration trajectory, and validate its role in migration through CRISPR/Cas9 deletion in two patient-derived models. ChIP-seq studies furthermore corroborate preferential TEAD1 binding at EGFR’s accessible regulatory elements. This validated multi-omic dataset enables further studies into tumor and microenvironment biology in the context of residual GBM disease.
2025-07-14 | GSE286413 | GEO
Project description:Glioblastoma (GBM) remains an untreatable disease. Understanding of GBM’s infiltrative biology at the resection margin is limited, despite causing disease recurrence and progression. To address this, we generated a high-throughput single-nucleus (sn)RNA-seq and snATAC-seq multi-omic dataset from six tumors with distinct genomic drivers and combined it with spatial transcriptomics to characterize the unique molecular phenotype of GBM near the margin. By contrasting GBM-specific biology in matching “Core” vs. “Margin” dissections, we define unique, shared “GBM infiltration” and chromatin accessibility signatures near the margin. We prioritize EGFR as a top differentially expressed and accessible “Margin” marker across GBM subtypes, show its dynamic expression along a core-to-margin infiltration trajectory, and validate its role in migration through CRISPR/Cas9 deletion in two patient-derived models. ChIP-seq studies furthermore corroborate preferential TEAD1 binding at EGFR’s accessible regulatory elements. This validated multi-omic dataset enables further studies into tumor and microenvironment biology in the context of residual GBM disease.
2025-07-14 | GSE286419 | GEO
Project description:We performed spatial transcriptomics on one IS-dominant tumor and on SLS-dominant tumor. Our goal was to determin different immune infiltration in these two subtypes.
2022-08-09 | GSE210755 | GEO
Project description:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that can cause gastrointestinal ulcers by affecting dopamine levels. Therefore, MPTP has been considered a toxic substance that causes gastric ulcer disease in experimental animals. In this study, tree shrews were used as the animal model of gastric mucosa injury, and MPTP was intraperitoneally injected for 13 weeks, while tree shrews were not injected as the control group. Under the light microscope, local congestion or diffuse bleeding points of gastric mucosa and multiple redness and swelling bleeding symptoms on the inner wall were observed in the treatment group, as well as immune cell infiltration was found in HE staining, but no such phenomenon was observed in the control group. In order to explore the molecular basis of changes in MPTP induced gastric mucosa injury, the transcriptome and proteome data of gastric mucosa were analyzed. We observed significant differences in mRNA and protein expression levels under the influence of MPTP. The changes in mRNA and proteins are related to increased immune infiltration, cellular processes and angiogenesis. More differentially expressed genes play a role in immune function, especially the candidate genes RPL4 and ANXA1 with significant signal and core role. There are also differentially expressed genes that play a role in mucosal injury and shedding, especially candidate genes GAST and DDC with certain signaling and corresponding functions. Understanding the factors and molecular basis that affect the expression of related genes is crucial for coping with Emotionality gastric mucosa injury disease and developing new treatment methods to establish the ability to resist disease.
2024-01-26 | PXD047458 | Pride