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RIPK1 kinase-dependent gene expression in human astrocytes in vitro

ABSTRACT: RIPK1 kinase-dependent gene expression in human astrocytes in vitro

PROVIDER: PRJNA724738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14316445.fastq.gz	Fastqsanger.gz
	SRR14316446.fastq.gz	Fastqsanger.gz
	SRR14316447.fastq.gz	Fastqsanger.gz
	SRR14316448.fastq.gz	Fastqsanger.gz
	SRR14316449.fastq.gz	Fastqsanger.gz

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Similar Datasets

RIPK1 kinase-dependent gene expression in human astrocytes in vitro

Project description:To determine the role of RIPK1 kinase-dependent transcriptional signaling in human fetal-derived astrocytes, we stimulated cells with the RIPK1 kinase-activating stimulus TNF/Smac/zVAD in the presence or absence of the RIPK1 kinase inhibitor Nec-1s. We identified various genes modulated in a RIPK1 kinase-dependent manner in human astrocytes, and the main biological pathways were related to an interferon signaling and anti-viral response.

2021-08-12 | GSE172027 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vitro

Project description:To determine the role of RIPK1 kinase-dependent transcriptional signaling in microglia and astrocytes, we stimulated cells with RIPK1 kinase-activating stimuli TNF/5z-7 and TNF/Smac/zVAD in the presence or absence of the RIPK1 kinase inhibitor Nec-1s. We identified various genes modulated in a RIPK1 kinase-dependent manner with each stimulation in both microglia and astrocytes, and the main biological pathways were related to an inflammatory and immune response. We identified many cytokines and chemokines upregulated in both microglia and astrocytes upon RIPK1 kinase activation, demonstrating the contribution of RIPK1 kinase signaling to pro-inflammatory responses in microglia and astrocytes

2021-08-12 | GSE154230 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. The top RIPK1 kinase-dependent gene pathways include oxidative phosphorylation and mitochondrial dysfunction in microglia and EIF2 signaling and cholesterol biosynthesis in astrocytes. This study demonstractes critical and distinct roles for RIPK1 kinase signaling in both microglia and astrocytes during EAE

2021-08-12 | GSE154228 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vitro

Project description:RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vitro

| PRJNA645451 | ENA

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

| PRJNA645447 | ENA

Genome wide Affymetric Microarray analysis for RIPK1 dependent inflammatory changes in Bone Marrow Derived Macrophages (BMDMs)

Project description:Gene level expression estimate using the Whole Transcript (WT) Assay approach of the Gene 1.0 ST Array System for Mouse. This assay was done to identify the RIPK1-dependent gene expression changes in mouse BMDMs. Cost-effective gene-level analysis based on whole-transcript coverage. We analyzed Bone Marrow Derived Macrophages (BMDMs) under 4 different conditions (Control, LPS, LPS/zVAD, LPS/zVAD/Nec-1) to assess inflammatory changes in RIPK1 kinase dependent manner compared to LPS, LPS/zVAD plus RIPK1 inhibitor Nec-1 and control.

2016-09-07 | E-GEOD-72797 | biostudies-arrayexpress

RIPK1 dephosphorylation and kinase activation by PPP1R3G/PP1γ promote apoptosis and necroptosis

Project description:Receptor-interacting protein kinase 1(RIPK1) is a key regulator of inflammation and cell death. Many sites on RIPK1, including serine 25, are phosphorylated to inhibit its kinase activity and cell death. How these inhibitory phosphorylation sites are dephosphorylated is poorly understood. Using a sensitized CRISPR whole genome knockout screen, we discover that protein phosphatase 1 regulatory subunit 3G (PPP1R3G) is required for RIPK1-dependent apoptosis and necroptosis. Mechanistically, PPP1R3G recruits its catalytic subunit protein phosphatase 1 gamma (PP1g) to Complex I to remove inhibitory phosphorylations of RIPK1. A PPP1R3G mutant which does not bind PP1g fails to rescue RIPK1 activation and cell death. Furthermore, chemical prevention of RIPK1 inhibitory phosphorylations or mutation of serine 25 of RIPK1 to alanine largely restores cell death in PPP1R3G-knockout cells. Finally, Ppp1r3g-/- mice are protected from tumor necrosis factor-induced systemic inflammatory response syndrome, confirming the important role of PPP1R3G in regulating apoptosis and necroptosis in vivo.

2021-10-26 | GSE176422 | GEO

Hepatocyte-Specific TAK1 Deficiency Drives RIPK1 Kinase-dependent Inflammation to Promote Liver Fibrosis and Hepatocellular Carcinoma

Project description:Transforming growth factor beta-activated kinase1 (TAK1) encoded by the gene MAP3K7 regulates multiple important downstream effectors involved in immune response, cell death and carcinogenesis. Hepatocyte-specific deletion of TAK1 in Tak1_Hep mice promotes liver fibrosis and hepatocellular carcinoma (HCC) formation. Here, we report that genetic inactivation of RIPK1 kinase using kinase dead knock-in D138N mutation in Tak1_Hep mice inhibits the expression of liver tumor biomarkers, liver fibrosis and HCC formation. Inhibition of RIPK1, however, has no or minimum effect on hepatocyte loss and compensatory proliferation, which are the recognized factors important for liver fibrosis and HCC development. Using single cell RNA-seq, we discover that inhibition of RIPK1 strongly suppresses inflammation induced by hepatocyte-specific loss of TAK1. Activation of RIPK1 promotes the transcription of key proinflammatory cytokines, such as CCL2, and CCR2+ macrophage infiltration. Our study demonstrates the role and mechanism of RIPK1 kinase in promoting inflammation, both cell-autonomously and cell-non-autonomously, in the development of liver fibrosis and HCC, independent of cell death and compensatory proliferation. We suggest the possibility of inhibiting RIPK1 kinase as a therapeutic strategy for reducing liver fibrosis and HCC development by inhibiting inflammation.

2020-07-08 | GSE148859 | GEO

Cooperation of TRADD- and RIPK1-dependent Cell Death Pathways in Maintaining Intestinal Homeostasis

Project description:Dysfunctional NF-kB signaling is critically involved in Inflammatory bowel disease (IBD). We investigated the mechanism by which RIPK1 and TRADD, two key mediators of NF-kB signaling, in mediating intestinal pathology using TAK1 IEC deficient model. We show that phosphorylation of TRADD by TAK1 modulates RIPK1-dependent apoptosis. TRADD and RIPK1 act cooperatively to mediate cell death mediated by TNF and TLR signaling. We demonstrate the pathological evolution from RIPK1-dependent ileitis to RIPK1- and TRADD-co-dependent colitis in TAK1 IEC deficient condition. Combined RIPK1 inhibition and TRADD knockout completely protect against intestinal pathology and lethality in TAK1 IEC KO mice. Furthermore, we identify distinctive microbiota dysbiosis biomarkers for RIPK1-dependent ileitis and TRADD-dependent colitis. These findings reveal the cooperation between RIPK1 and TRADD in mediating cell death and inflammation in IBD with NF-kB deficiency and suggest the possibility of combined RIPK1 kinase inhibition and TRADD knockout as a new therapeutic strategy for IBD.

2025-01-22 | GSE279034 | GEO

Next Generation Sequencing to check the enrichment of RIPK1/BAF on chromatin, RIPK1-dependent chromatin state and RIPK1-dependent transcriptome during inflammatory responses.

Project description:RIPK1 is a master regulator of multiple cell death pathways, including apoptosis and necroptosis, and inflammation. Multiple RIPK1 inhibitors have been advanced into human clinical trials as new therapeutics for human inflammatory and neurodegenerative diseases, including ALS and AD. However, while the mechanism of cytosolic RIPK1 in control of cell death has been extensively investigated, how the activation of RIPK1 may promote transcription of proinflammatory cytokines is unclear as a nuclear function of RIPK1 has not been explored, nor is it clear if and how RIPK1 kinase activity may directly mediate inflammation independent of cell death. Here we show that nuclear RIPK1 is recruited by specific transcription factors and binds to the BAF complex on active enhancers and promoters marked by H3K4me1 and H3K27ac. Nuclear RIPK1 mediates the phosphorylation of SMARCC2, a key component of the BAF complex, to promote chromatin remodeling and the transcription of specific proinflammatory genes. Our results suggest that RIPK1 kinase serves a transcriptional coregulator in nucleus that can transmit extracellular stimuli to BAF complex to modulate the chromatin accessibility and directly regulate the transcription of specific genes involved in mediating inflammatory responses.

2022-07-13 | GSE179018 | GEO

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