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RNA-seq in RAW264.7 cells after silence of Synbindin in response to LPS

ABSTRACT: RNA-seq in RAW264.7 cells after silence of Synbindin in response to LPS

PROVIDER: PRJNA664772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12682984_1.fastq.gz	Fastqsanger.gz
	SRR12682984_2.fastq.gz	Fastqsanger.gz
	SRR12682985_1.fastq.gz	Fastqsanger.gz
	SRR12682985_2.fastq.gz	Fastqsanger.gz
	SRR12682986_1.fastq.gz	Fastqsanger.gz

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RNA-seq in RAW264.7 cells after silence of Synbindin in response to LPS

Project description:RAW264.7 cells were transfected with Synbindin siRNA for 48hours, then 100ng/ml LPS were treated cells for 4 hours. Before and after LPS stimulation, cells were collected and RNA were extracted for RNA-seq.

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LPS stimulated murine RAW264.7 cells, incubated with DMSO carrier or mycolactone

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AF9/MLLT3 ChIP-Seq in LPS-stimulated RAW264.7 cells

Project description:We sought to characterize the genomic localization of the YEATS domain protein AF9 in the macrophage-like cell line RAW 264.7 +/- LPS stimulation and +/- sodium crotonate pretreatment. We performed chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq) for endogenous AF9 or for a FLAG-tagged AF9 transgene in RAW264.7 or a RAW264.7 cell line engineered to express FLAG-AF9, respectively.

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Project description:Unanticipated regulatory protein modifications can be discovered from the unbiased comprehensive analysis of biological systems using SAMPEI. To explore this idea, we sought to map protein modifications induced during mammalian cell differentiation, modeled by the response of mouse RAW264.7 macrophage cells to lipopolysaccharide (LPS), a potent inducer of macrophage activation and differentiation that involves extensive protein and metabolic signaling.

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Project description:After stimulation of RAW264.7 cells with LPS and Harmine, high-throughput sequencing technology was used to explore the changes in the inflammation level of RAW cells and the enrichment of signaling pathways after LPS and Harmine treatment, and to find an interesting target pathway.

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H3K4methylation in Setd1a loss-of-function Raw264.7 cells upon LPS or Dex+LPS stimulation

Project description:Nuclear interaction studies by ChIP coupled with mass spectrometry identified the COMPASS/SETD1A complex as interaction partner of the glucocorticoid receptor (GR) in murine bone marrow-derived macrophages (BMDMs). Here, we profiled H3K4me1, H3K4me2 and H3K4me3 in wild-type and Setd1a hypermorphic (Setd1aDel/+) Raw264.7 cells after LPS and Dex+LPS stimulation by spike-in ChIP-Seq.

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Role of RUVBL2 in LPS-induced proinflammatory gene expression of RAW264.7 cells

Project description:The aim of this experiment is to compare gene expression proflies of RAW264.7 cells trasnfected with non-targeting siRNA or siRNA against RUVBL2, in the presence or absence of LPS.

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miRNA profiling in RAW264.7 cells treated without or with LPS and IFNγ

Project description:We have identified a number of miRNAs that are differentially expressed in LPS and IFNγ treated RAW264.7 cells, as compared to untreated cells. Microarray and quantitative real-time PCR (qRT-PCR) results showed that miR-103 decreased while the STAT1 expression increased substantially in RAW264.7 derived M1 macrophage, and there was a significant negative correlation between miR-103 and STAT1.Overexpression of miR-103 suppressed M1 polarization by inhibiting STAT1/IRF1 signaling pathway and vice versa in vitro. STAT1 is a direct target of of miR-103.

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Ribo-Seq timecourse in RAW264.7 cells upon LPS treatment

Project description:Ribo-Seq timecourse in RAW264.7 cells upon LPS treatment

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Transcriptome profiles of RAW264.7 cells under fibroblast coculture with or without LPS sitimulation and tryptophan metabolites intervention

Project description:We performed RNA sequencing to identify the role of fibroblast in the effects of tryptphan metabolites on LPS-stimulated RAW264.7 cells.

2025-05-13 | GSE279383 | GEO

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