Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer

ABSTRACT: RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer

PROVIDER: PRJNA437634 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6821770_1.fastq.gz	Fastqsanger.gz
	SRR6821770_2.fastq.gz	Fastqsanger.gz
	SRR6821771_1.fastq.gz	Fastqsanger.gz
	SRR6821771_2.fastq.gz	Fastqsanger.gz
	SRR6821772_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer

Project description:Gene ontology analysis suggested that targeting RIP1 induced changes in diverse innate inflammatory processes. Ingenuity analysis demonstrated that pathwaysupregulated by RIP1i included both MAP kinase and PPAR signaling, whereas select apoptosis and phagocytosis pathways were inhibited.

2018-09-10 | GSE111626 | GEO

RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer.

Project description:Pancreatic ductal adenocarcinoma (PDA) is characterized by immune tolerance and immunotherapeutic resistance. We discovered upregulation of receptor-interacting serine/threonine protein kinase 1 (RIP1) in tumor-associated macrophages (TAMs) in PDA. To study its role in oncogenic progression, we developed a selective small-molecule RIP1 inhibitor with high in vivo exposure. Targeting RIP1 reprogrammed TAMs toward an MHCIIhiTNFα+IFNγ+ immunogenic phenotype in a STAT1-dependent manner. RIP1 inhibition in TAMs resulted in cytotoxic T cell activation and T helper cell differentiation toward a mixed Th1/Th17 phenotype, leading to tumor immunity in mice and in organotypic models of human PDA. Targeting RIP1 synergized with PD1-and inducible co-stimulator-based immunotherapies. Tumor-promoting effects of RIP1 were independent of its co-association with RIP3. Collectively, our work describes RIP1 as a checkpoint kinase governing tumor immunity.

| S-EPMC6836726 | biostudies-literature

Genetic inactivation of RIP1 kinase activity in rats protects against ischemic brain injury

Project description:RIP1 kinase-mediated inflammatory and cell death pathways have been implicated in the pathology of acute and chronic disorders of the nervous system. Here, we describe a novel animal model of RIP1 kinase deficiency, generated by knock-in of the kinase-inactivating RIP1(D138N) mutation in rats. Homozygous RIP1 kinase-dead (KD) rats had normal development, reproduction and did not show any gross phenotypes at baseline. However, cells derived from RIP1 KD rats displayed resistance to necroptotic cell death. In addition, RIP1 KD rats were resistant to TNF-induced systemic shock. We studied the utility of RIP1 KD rats for neurological disorders by testing the efficacy of the genetic inactivation in the transient middle cerebral artery occlusion/reperfusion model of brain injury. RIP1 KD rats were protected in this model in a battery of behavioral, imaging and histopathological endpoints. In addition, RIP1 KD rats had reduced inflammation and accumulation of neuronal injury biomarkers. Unbiased proteomics in the plasma identified additional changes that were ameliorated by RIP1 genetic inactivation. Together these data highlight the utility of the RIP1 KD rats for target validation and biomarker studies for neurological disorders. For mass spectrometry experiment, please check the method section in the manuscript.

2020-12-21 | MSV000086623 | MassIVE

RIP1 perturbation induces chondrocyte necroptosis and promotes osteoarthritis pathogenesis

Project description:Receptor-interacting protein kinase 1 (RIP1)-mediated necroptosis plays a vital role in various diseases, but the involvement of RIP1 and its functional mechanism in osteoarthritis pathogenesis remains largely unknown. To identify molecular targets of RIP1 in chondrocytes, RNA sequencing was performed in chondrocytes treated with adenovirus expressing RIP1 or vector control. We found that 9857 genes were differentially expressed in chondrocytes after RIP1 overexpression. GO analysis indicated that DNA replication, chromosome segregation and regulation of cell cycle process were upregulated, while terms including cartilage development, skeletal system development, extracellular matrix organization, skeletal system morphogenesis, chondrocyte differentiation, collagen fibril organization and limb development were downregulated. Pathway analysis revealed that IL-17 signaling pathway, cell cycle, DNA replication, proteasome, TNF signaling pathway, cellular senescence and p53 signaling pathway were significantly upregulated by RIP1, meanwhile, ECM-receptor interaction, other glycan degradation and glycosaminoglycan degradation were downregulated. These results underscore the importance of RIP1 in OA by perturbing a series of essential events during disease progression such like cell cycle regulation, chondrocyte differentiation, inflammation and ECM remodeling.

2021-01-22 | GSE165219 | GEO

The Rip1 cytochrome bc1 catalytic subunit modulates antifungal tolerance in Candida auris

Project description:Comparative transcriptomic profiling of Candida auris rip1∆ and WT

2025-09-19 | GSE308547 | GEO

The Rip1 cytochrome bc1 catalytic subunit modulates antifungal tolerance in Candida auris

Project description:The Rip1 cytochrome bc1 catalytic subunit modulates antifungal tolerance in Candida auris

| PRJNA1330857 | ENA

Histone deacetylase 3 facilitates TNF α -mediated NF-κB activation through suppressing CTSB induced RIP1 degradation and is required for host defense against bacterial infection

Project description:Histone deacetylases (HDACs), as important enzymes regulating acetylation, participate in a series of cell physiological process. Here we reported that HDAC3-deficient macrophages had elevated expression of multiple cathepsins and over-expressed cathepsins such as cathepsin B (CTSB) caused remarkable degradation of receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIP1), which resulted in reduced TNFα mediated NF-κB activation and inflammatory response. Consistent with these findings, mice with macrophage specific knockout of HDAC3 were impaired in inflammatory response and susceptible to pseudomonas aeruginosa infection. Thus, our studies uncovered important roles of HDAC3 in the regulation of cathepsin-mediated lysosomal degradation and RIP1-mediated inflammatory response in macrophages as well as in host defense against bacterial infection.

2022-05-12 | GSE197989 | GEO

Histone deacetylase 3 facilitates TNF α -mediated NF-κB activation through suppressing CTSB induced RIP1 degradation and is required for host defense against bacterial infection [ChIP-seq]

2022-05-12 | GSE198218 | GEO

Transcriptional profiling of macrophage plasticity following recovery from Lipopolysaccharide (LPS) tolerance

Project description:To investigate the plasticity of Lipolysaccharide (LPS) tolerance, we employed microarray profiling to analyse the gene expression profile in macrophage. Four macrophage populations were induced; Untreated macrophages (Control group), Acute response to LPS (LPS activation group), LPS tolerance (T – Tolerant group) and recovered (R = recovered macrophage group) Using transcriptional analysis we demonstrate that recovery from LPS tolerance (R – Recovery), as defined by cytokine gene expression, is associated with a global change in the transcriptional profile of macrophage. This data confirms that LPS tolerance is a transient state which results in induction of novel hybrid macrophage activation state with a unique transcriptional signature. Bone marrow derived macrophages were polarised into three activation states; Acute response to LPS (A), LPS tolerant (T) and recovered (R). Gene expression was measured at 4 hours post stimulation with LPS. Three independent experiments were performed to measure gene expression changes between each macrophage group.

2013-12-06 | E-GEOD-47783 | biostudies-arrayexpress

Transcriptional profiling of macrophage plasticity following recovery from Lipopolysaccharide (LPS) tolerance

2013-12-06 | GSE47783 | GEO