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Mus musculus

ABSTRACT: H3K18Ac and H3K18Cr ChIP-seq and RNA-seq analysis of LPS-stimulated RAW 264.7 cells

PROVIDER: PRJNA269347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1694050.fastq.gz	Fastqsanger.gz
	SRR1694051.fastq.gz	Fastqsanger.gz
	SRR1694052.fastq.gz	Fastqsanger.gz
	SRR1694053.fastq.gz	Fastqsanger.gz
	SRR1694054.fastq.gz	Fastqsanger.gz

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CstF-64 Influenced Gene Expression

Project description:Triplicate samples of RAW 264.7 murine macrophages either untreated, stimulated with 100 ng/ml LPS for 18 hours, or constituitively over-expressing CstF-64 were analyzed by microarray using Affymetrix murine gene chip 430A. Keywords = RAW 264.7 macrophages Keywords = LPS Keywords = CstF-64 Keywords: repeat sample

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Identification of Nucleolin-binding targets and sequences in LPS-stimulated RAW 264.7 cells by PAR-CLIP

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Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [RNA-seq]

Project description:The involvement of m6A modification in macrophage activation has been validated in our study that the expression of TNF-α in Mettl3-depleted Raw 264.7 cells stimulated with LPS were markedly reduced in comparison to control cells. To further explore the biological effects of m6A deficiency macrophages, we performed RNA sequencing analysis of Mettl3-KO and WT control Raw 264.7 cells upon LPS treatment. The GO enrichment analysis documented that the downregulated transcripts in Mettl3-KO Raw 264.7 cells were enriched in innate immune response related to defense and external stimulus. Notably, transcripts of the downstream components of the TLR4 signaling pathway, such as proinflammatory cytokines (Tnf-α, Il-6, Il-1β, Il-18,and Il-23) and co-stimulation molecules (Cd86), were downregulated in Mettl3-deficient cells, suggesting that METTL3 has a critical function in controlling the innate immune response of Raw 264.7 macrophages.

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Expression Profiles of 15(S)-HETE treated RAW 264.7 cells

Project description:Hemozoin phagocytosis results in immunomodulation. This study was designed to explore gene expression responses to 15(S)-HETE in LPS-stimulated RAW 264.7 cells.

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Next Generation Sequencing of Wild Type and Hnrnpul1-/- RAW 264.7 Cells Transcriptomes

Project description:Purpose: The goal of this study is to compare NGS-derived wild type and Hnrnpul1 knockout (Hnrnpul1-/-) RAW 264.7 cells transcriptomes with or without LPS stimulation. Methods: Sequancing was performed by Novogene China Co. Ltd. RNA profiles of wild type and Hnrnpul1-/- RAW 264.7 cells as well as LPS stimulated (10 h) wild type and Hnrnpul1-/- RAW 264.7 cells were generated by deep sequencing using Illumina Novaseq 6000. Index of the reference genome was built using Hisat2 v2.0.5 and paired-end clean reads were aligned to the reference genome using Hisat2 v2.0.5. featureCounts v1.5.0-p3 was used to count the reads numbers mapped to each gene. And then FPKM of each gene was calculated based on the length of the gene and reads count mapped to this gene. Method of TMM was used to normalize the readcount. Negative binomial distribution model was used to calculate the P value, and FDR was calculated by the method of Benjaminiand Hochberg. Results: Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the mouse genome (GRCm38/mm10). Comparing to wild type RAW 264.7 cells, 237 genes were up-regulated and 181 genes were down-regulated in Hnrnpul1-/- cells. At 10 h following LPS stimulation, 341 genes were up-regulated and 288 genes were down-regulated in Hnrnpul1-/- cells. Genes were pre-ranked according to log2FoldChange(KO/WT) followed by GSEA and 6 gene sets were significantly enriched. Significantly differential genes were undergone GO analysis (biological process) and biological process including cell-cell adhesion, positive regulation of cell activation and regulation of response to external stimulus were enriched. Conclusions: Lacking Hnrnpul1 promotes the expression of inflammatory cytokines in LPS stimulated RAW 264.7 cells.

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Project description:LPS stimulation of Mouse (RAW 264.7) macrophages

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