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ULK1-dependent phosphorylation of RIPK1 within the intermediate domain

ABSTRACT: Mass-spectrometric analysis of an in vitro kinase assay using recombinant active ULK1 (Sigma-Aldrich, SRP5096) as kinase and GST-RIPK1(250-475) as substrate

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Björn Stork

LAB HEAD: Björn Stork

PROVIDER: PXD018035 | Pride | 2020-04-22

REPOSITORIES: Pride

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Publications

The Autophagy-Initiating Kinase ULK1 Controls RIPK1-Mediated Cell Death.

Wu Wenxian W Wang Xiaojing X Berleth Niklas N Deitersen Jana J Wallot-Hieke Nora N Böhler Philip P Schlütermann David D Stuhldreier Fabian F Cox Jan J Schmitz Katharina K Seggewiß Sabine S Peter Christoph C Kasof Gary G Stefanski Anja A Stühler Kai K Tschapek Astrid A Gödecke Axel A Stork Björn B

Cell reports 20200401 3

Autophagy, apoptosis, and necroptosis are stress responses governing the ultimate fate of a cell. However, the crosstalk between these cellular stress responses is not entirely understood. Especially, it is not clear whether the autophagy-initiating kinase ULK1 and the cell-death-regulating kinase RIPK1 are involved in this potential crosstalk. Here, we identify RIPK1 as a substrate of ULK1. ULK1-dependent phosphorylation of RIPK1 reduces complex IIb/necrosome assembly and tumor necrosis factor ...[more]

PMID: 32320653

Similar Datasets

ULK1-dependent phosphorylation of RIPK1 within the intermediate domain

Project description:Mass-spectrometric analysis of an in vitro kinase assay using recombinant active ULK1 (Sigma-Aldrich, SRP5096) as kinase and GST-RIPK1(250-475) as substrate

2020-04-22 | PXD018078 | Pride

Central Role of ULK1 in Type I Interferon Signaling

Project description:We provide evidence that the Unc-51-like kinase 1 (ULK1) is phosphorylated and activated during engagement of the Type I IFN receptor. Our studies demonstrate that the function of ULK1 controls expression of key interferon stimulated genes (ISGs) that mediate important biological functions, including anti-viral and antineoplastic responses. Total RNA was isolated from untreated and IFNβ-treated Ulk1/2+/+ and Ulk1/2-/- mouse embryonic fibroblasts (MEFs). Cells were treated for 6 hours with or without mouse IFNβ (2500 IU/ml).

2014-08-26 | E-GEOD-60778 | biostudies-arrayexpress

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.

2022-10-20 | GSE193509 | GEO

Central Role of ULK1 in Type I Interferon Signaling

2014-08-26 | GSE60778 | GEO

Fumarate hydratase orchestrates hepatic steatosis via ULK1 mediated lipophagy

Project description:Hepatic lipid homeostasis is coordinated by various metabolic pathways, such as lipogenesis, lipid uptake, storage, and oxidation. However, the underlying mechanism that orchestrates metabolic crosstalk remains unclarified. Herein, we demonstrated that fumarate hydratase (FH) functioned as an indispensable adaptor governing mitochondria metabolism and lipid droplets (LDs) degradation. Hepatic FH overexpression prevented hepatic steatosis in normal mice and ob/ob mice without interfering mitochondrial lipid oxidation and lipogenesis. Strikingly, we found that FH selectively activated lipophagy-mediated LDs lipidolysis. Mechanistically, FH interacted with ULK1 and stabilized ULK1 through preventing its ubiquitination and degradation, resulting in lipophagy activation and the elimination of hepatic lipid accumulation. Meanwhile, hepatic ULK1 deficiency abrogated the protective effects in FH-overexpressing mice. Also, we clarified that the interaction between FH and ULK1 occurred in cytoplasm, but not in mitochondria. Cytoplasmic FH was sensitive to lipids and downregulated without affecting mitochondrial FH in vivo. Moreover, the FH-ULK1 axis was identified closely associated with hepatic steatosis in human patients. Taken together, our research demonstrates a “two-side” insight of FH on hepatic lipid metabolism and provides a promising strategy for fatty liver treatment.

2024-02-26 | GSE256510 | GEO

Expression data from Ulk1 silencing in mouse liver and AML12 cells

Project description:This experiments detail the differential gene expressionin hepatic cells in response to Ulk1 silencing both in vivo and in vitro We used microarrays to detail the global programme of gene expression underlying the loss of ULK1 knockdownin hepatic cells

2020-03-27 | GSE147579 | GEO

Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA

Project description:Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA shows differential effect of Ulk1 KD on LXr responsive genes AML-12 cells co-treated with 0.75mM PA+/- 10ÂµM GW3965 for 24 h +/- Ulk1 SiRNA

2016-03-31 | E-GEOD-74059 | biostudies-arrayexpress