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Screening RIPK3 dependent signaling pathway and genes expression in intestinal GVHD mice models

ABSTRACT: Screening RIPK3 dependent signaling pathway and genes expression in intestinal GVHD mice models

PROVIDER: PRJNA695374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13559358_1.fastq.gz	Fastqsanger.gz
	SRR13559358_2.fastq.gz	Fastqsanger.gz
	SRR13559359_1.fastq.gz	Fastqsanger.gz
	SRR13559359_2.fastq.gz	Fastqsanger.gz
	SRR13559360_1.fastq.gz	Fastqsanger.gz

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Screening RIPK3 dependent signaling pathway and genes expression in intestinal GVHD mice models

Project description:Lethally irradiated recipient C57BL/6 WT, RIPK3-/- and Villin-cre RIPK3fl/fl mice received Balb/c bone marrow and CD4+ T cells. After 17 days, total RNA was extracted from small intestine and deep sequenced to compare the gene expression profiles among WT, RIPK3-/- and Villin-cre RIPK3fl/fl.

2021-01-28 | GSE165606 | GEO

Screening regulated pathway and genes expression in intestinal GVHD patients

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Screening regulated pathway and genes expression in intestinal GVHD patients

Project description:Screening regulated pathway and genes expression in intestinal GVHD patients

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Genomic locus proteomic screening identifies the NF-kB signaling pathway components NFkB1 and IKBKG as transcriptional regulators of Ripk3 in endothelial cells

Project description:The receptor-interacting protein kinase 3 (RIPK3) is a multi-functional protein best known for facilitating cellular necroptosis and inflammation. Recent evidence from our lab indicates that RIPK3 expression must be tightly regulated in endothelial cells to promote angiogenesis and maintain vascular integrity during embryogenesis and to provide protection from postnatal atherosclerosis. RIPK3 activity and stability are regulated by post-translational modifications and caspase-dependent cleavage. However, less is known about the transcriptional regulation of Ripk3. Here we utilized an unbiased CRISPR-based technology called genomic locus proteomics (GLoPro) to screen transcription factors and coregulatory proteins associated with the Ripk3 locus in a murine endothelial cell line. We found that 41 nuclear proteins are specifically enriched at the Ripk3 locus, including the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway components NFkB1 and IKBKG. We further verified that NFkB1 and IKBKG directly bind the Ripk3 promoter and prevent TNFa-induced Ripk3 transcription in cultured human primary endothelial cells. Moreover, NFkB1 prevents RIPK3-mediated death of primary endothelial cells. These data provide new insights into NF-kB signaling and Ripk3 transcriptional regulation in endothelial cells.

2021-06-09 | PXD025675 | Pride

Genes expression in intestinal GVHD

Project description:Genes expression in intestinal GVHD

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Transcriptional profiles of PA1 teratoma cells transfected by RIPK1, RIPK2, RIPK3, or RIPK4

Project description:RIPK4 but not the related kinases RIPK1, RIPK2, and RIPK3 caused similar transcriptional changes to Wnt3a. PA1 cells were transfected by 8ug RIPK1, RIPK2, RIPK3, or RIPK4 for 48h, RNA were extracted and sequenced.

2013-02-04 | E-GEOD-43362 | biostudies-arrayexpress

Ubiquitylation of RIPK3 beyond-the-RHIM limits RIPK3 activity and cell death

Project description:Pathogen recognition receptors and TNF superfamily members engage Receptor Interacting Serine/threonine Kinase-3 (RIPK3) to activate programmed cell death, including MLKL-mediated necroptosis and caspase-8-dependent apoptosis. However, the post-translational control of RIPK3 signalling is not fully understood. Using mass-spectrometry, we identified a novel ubiquitylation site on murine RIPK3 beyond the RIP homotypic interaction motif (RHIM) on K469. Complementation of RIPK3-deficient cells with a Ripk3K469R mutant demonstrated that the decoration of RIPK3 K469 by ubiquitin limits both RIPK3-mediated caspase-8 activation and apoptotic killing, in addition to RIPK3 autophosphorylation and MLKL-mediated necroptosis. Unexpectedly, the overall ubiquitylation of mutant RIPK3K469R was enhanced, which largely resulted from additional RIPK3 ubiquitylation on K359. Loss of RIPK3 K359 ubiquitylation reduced RIPK3K469R hyper-ubiquitylation and limited the ability of Ripk3K469R/K469R to trigger enhanced killing. Ripk3K469R/K469R mice challenged with Salmonella displayed increased bacterial loads in the spleen and liver, with reduced IFN serum levels. Therefore, RIPK3 K469 ubiquitylation can function to prevent RIPK3 ubiquitylation on alternate lysine residues, which otherwise promote RIPK3 oligomerization and consequent cell death signalling.

2022-08-12 | PXD026533 | Pride

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2018-11-06 | GSE122121 | GEO

Neuronal DAMPs exacerbate neurodegeneration via astrocytic RIPK3 signaling

Project description:Astrocyte activation is a common feature of neurodegenerative diseases. However, the ways in which dying neurons influence the activity of astrocytes is poorly understood. RIPK3 signaling has recently been described as a key regulator of neuroinflammation, but whether this kinase mediates astrocytic responsiveness to neuronal death has not yet been studied. Here, we used the MPTP model of Parkinson’s disease to show that activation of astrocytic RIPK3 drives dopaminergic cell death and axon damage. Transcriptomic profiling revealed that astrocytic RIPK3 promoted gene expression associated with neuroinflammation and movement disorders, and this coincided with significant engagement of DAMP signaling. Using human cell culture systems, we show that factors released from dying neurons signal through RAGE to induce RIPK3-dependent astrocyte activation. These findings highlight a mechanism of neuron-glia crosstalk in which neuronal death perpetuates further neurodegeneration by engaging inflammatory astrocyte activation via RIPK3.

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