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Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_iRIP-seq)

ABSTRACT: Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_iRIP-seq)

PROVIDER: PRJNA555344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9708010_1.fastq.gz	Fastqsanger.gz
	SRR9708010_2.fastq.gz	Fastqsanger.gz
	SRR9708011_1.fastq.gz	Fastqsanger.gz
	SRR9708011_2.fastq.gz	Fastqsanger.gz
	SRR9708012_1.fastq.gz	Fastqsanger.gz

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Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability

Project description:Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability

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Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_OE_RNA-seq)

Project description:Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_OE_RNA-seq)

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Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_OE_RNA-seq)

Project description:We overexpressed Prdx1 in HeLa cells to study Prdx1-regulated genes using RNA-seq technology, followed by bioinformatic analysis of target genes of Prdx1-regulated.

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Prdx1,a RNA binding protein,regulate inflammatory injury in intracerebral hemorrhage by targeting RNA stability (PRDX1_iRIP-seq)

Project description:We overexpressed Prdx1 in HeLa cells to study Prdx1-regulated genes using RNA-seq technology, followed by bioinformatic analysis of target genes of Prdx1-regulated.In order to find the precise regulatory mechanisms,we performed iRIP-seq experiment in HeLa cell.

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Examining Transcriptomic Alterations in Rat Models of Intracerebral Hemorrhage and Severe Intracerebral Hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a life-threatening condition associated with significant morbidity and mortality. Understanding the molecular mechanisms underlying ICH and its severe form is crucial for developing effective therapeutic strategies. This study investigates transcriptomic alterations in rodent models of ICH and severe intracerebral hemorrhage to shed light on the genetic pathways involved in hemorrhagic brain injury. We performed principal component analysis, revealing distinct principal component segments of normal rats compared to intracerebral hemorrhage and severe intracerebral hemorrhage rats. We further employed heatmaps and volcano plots to identify differentially expressed genes and utilized bar plots and KEGG pathway analysis to elucidate the different molecular pathways involved. Using comprehensive RNA sequencing and bioinformatics analyses, we identified a multitude of differentially expressed genes in both the ICH and severe ICH models. Our results revealed 5679 common genes among the normal, intracerebral hemorrhage, and severe intracerebral hemorrhage groups in the upregulated genes group, and 1196 common genes in the downregulated genes. A volcano plot comparing the groups further highlighted common genes, including PDPN, TIMP1, SERPINE1, TUBB6, and CD44. These findings underscore the complex interplay of genes involved in inflammation, oxidative stress, and neuronal damage. Furthermore, pathway enrichment analysis uncovered key signaling pathways, including the TNF signaling pathway, protein processing in the endoplasmic reticulum, MAPK signaling pathway, and Fc gamma R-mediated phagocytosis, implicated in the pathogenesis of ICH.

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Analysis of Age-Dependent Transcriptomic Changes in Response to Intracerebral Hemorrhage in Mice

Project description:To investigate age-dependent transcriptomic changes between young or aged intracerebral hemorrhage mice, we established collagenase IV-induced intracerebral hemorrhage mice models. Intracerebral hemorrhage was induced by infusion of sterile collagenase IV in ipsilateral caudate putamen of brain. We then performed gene expression profiling analysis using data obtained from RNA-seq of brain perihematomal tissues from young or aged ICH mice 24 hours after intracerebral hemorrhage.

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2024-08-22 | E-MTAB-14351 | biostudies-arrayexpress

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