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T cell-specific RIPK1 ablation results in villus atrophy of the duodenum in mice

ABSTRACT: T cell-specific RIPK1 ablation results in villus atrophy of the duodenum in mice

PROVIDER: PRJNA1100505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28696870_1.fastq.gz	Fastqsanger.gz
	SRR28696870_2.fastq.gz	Fastqsanger.gz
	SRR28696871_1.fastq.gz	Fastqsanger.gz
	SRR28696871_2.fastq.gz	Fastqsanger.gz
	SRR28696872_1.fastq.gz	Fastqsanger.gz

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T cell-specific RIPK1 ablation results in villus atrophy of the duodenum in mice

Project description:RIPK1 is required in T cells with a history of CD4-expression to maintain intestinal homeostasis. We show that the pathology in the upper intestine is a result of conventional T cell apoptosis in absence of the RIPK1.

2025-03-05 | GSE263990 | GEO

Gene expression profile of mouse intestinal epithelial cells during homeostasis and villus atrophy

Project description:The epithelium that lines small intestinal villi is critically important for nutrient absorption, defense against pathogens, and mucosal homeostasis. Atrophy or blunting of the villi as a result of epithelial damage is commonly observed in celiac disease, viral gastroenteritis, and various other pathologies. Whereas adaptive responses during epithelial stem cell injury are increasingly well understood, how epithelial tissues, and particularly the intestine, cope with drastic loss of differentiated cells remains unclear. Using an acute model of viral gastroenteritis induced by poly(I:C), we aimed to dissect the cellular adaptations that follow severe intestinal villus injury.

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Gene expression profile of mouse intestinal epithelial cells during homeostasis and villus atrophy at single-cell resolution

2021-03-27 | GSE169718 | GEO

Gene expression profile of mouse intestinal epithelial cells during homeostasis and villus atrophy

Project description:Gene expression profile of mouse intestinal epithelial cells during homeostasis and villus atrophy

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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

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

Quantitative Transcriptome Analysis of RIPK1-KO CD4 T cells

Project description:RIPK1 is a key signaling molecule controlling cell death and inflammation through both scaffold and kinase functions of RIPK1. Human RIPK1 deficiency causes immunodeficiency and inflammatory diseases. Here we analyzed the functional roles of RIPK1 in CD4 T cells.

2022-02-27 | GSE197232 | GEO

SENP1 prevents steatohepatitis by suppressing RIPK1-driven apoptosis and inflammation

Project description:The mechanism underlying RIPK1-driven cell death and inflammation, a key process in the progression of nonalcoholic steatohepatitis, remains unclear. Here we identified SENP1, a SUMO-specific protease, as a key endogenous inhibitor of RIPK1. SENP1 is progressively reduced in proportion to NASH severity in patients. Hepatocyte-specific SENP1-knockout mice develop spontaneous NASH-related phenotypes in a RIPK1 kinase-dependent manner. We demonstrate that SENP1 deficiency sensitizes cells to RIPK1 kinase-dependent apoptosis by promoting RIPK1 activation following TNFα stimulation. Mechanistically, SENP1 deSUMOylates RIPK1 in TNF-R1 signaling complex (TNF-RSC), keeping RIPK1 in check. Loss of SENP1 leads to SUMOylation of RIPK1, which re-orchestrates TNF-RSC and modulates the ubiquitination patterns and activity of RIPK1. Notably, genetic inhibition of RIPK1 effectively reverses disease progression in hepatocyte-specific SENP1-knockout male mice with high-fat-diet-induced nonalcoholic fatty liver. We propose that deSUMOylation of RIPK1 by SENP1 provides a pathophysiologically relevant cell death-restricting checkpoint that modulates RIPK1 activation in the pathogenesis of nonalcoholic steatohepatitis.

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insulin resistant duodenum vs. non-insulin resistant duodenum

Project description:insulin resistant duodenum vs. non-insulin resistant duodenum

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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

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