Project: Autophagy in inflammation and inflammatory disorders (ATLANTIS), from basic insights to experimental therapy
2021-01-01 – 2024-12-31
- Abstract
Autophagy is crucial in the (patho)physiology, including inflammation, infection and cancer. Autophagy functions as a survival mechanism by maintaining viability during periods of stress, and by removing damaged organelles and toxic metabolites, such as protein aggregates or intracellular pathogens. The Atlantis research consortium (AuTophagy in InfLAmmatioN and inflammaTory dISorders) brings together a team of expert investigators from the complementary fields of autophagy, (cancer) cell death signaling, inflammation signaling, angiogenesis and atherosclerosis, and drug screening and medicinal chemistry. We will study in an integrated way the impact of autophagy and its pharmacological modulation in various vascular diseases with a focus on the endothelium and its functional interaction with immune cells in sepsis, tumor-driven (lymph)angiogenesis, and atherosclerosis.
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Type 1 immunity enables neonatal thymic ILC1 production
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Decoding immunogenic cell death from a dendritic cell perspective
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A guide to the expanding field of extracellular vesicles and their release in regulated cell death programs
(2024) FEBS JOURNAL. -
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Tumor endothelial cell autophagy is a key vascular-immune checkpoint in melanoma
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NINJ1 is activated by cell swelling to regulate plasma membrane permeabilization during regulated necrosis
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Systematic compositional analysis of exosomal extracellular vesicles produced by cells undergoing apoptosis, necroptosis and ferroptosis
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Cell death checkpoints in the TNF pathway
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Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression
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Inhibition of RIPK1 kinase does not affect diabetes development : beta-cells survive RIPK1 activation
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From PERK to RIPK1 : design, synthesis and evaluation of novel potent and selective necroptosis inhibitors
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LC3-independent autophagy is vital to prevent TNF cytotoxicity
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Death by TNF : a road to inflammation
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Molecular mechanisms of nemorosone-induced ferroptosis in cancer cells
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RIPK1 kinase-dependent inflammation and cell death contribute to the pathogenesis of COPD
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Pore-forming proteins as drivers of membrane permeabilization in cell death pathways
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Tyramide signal amplification for the immunofluorescent staining of ZBP1-dependent phosphorylation of RIPK3 and MLKL after HSV-1 infection in human cells
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ATG9A prevents TNF cytotoxicity by an unconventional lysosomal targeting pathway.
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Phosphorylation of RIPK1 serine 25 mediates IKK dependent control of extrinsic cell death in T cells
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Spectrally tunable Förster resonance energy transfer-based biosensors using organic dye grafting
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ADAR1 prevents autoinflammation by suppressing spontaneous ZBP1 activation
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Cancer cells dying from ferroptosis impede dendritic cell-mediated anti-tumor immunity
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Association of cell death markers with tumor immune cell infiltrates after chemo-radiation in cervical cancer
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MLKL deficiency in BrafV600EPten-/- melanoma model results in a modest delay of nevi development and reduced lymph node dissemination in male mice
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Reduced protection of RIPK3-deficient mice against influenza by matrix protein 2 ectodomain targeted active and passive vaccination strategies
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Executioner caspases 3 and 7 are dispensable for intestinal epithelium turnover and homeostasis at steady state
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Plasma membrane perforation by GSDME during apoptosis-driven secondary necrosis