Publications by authors named "F Schorn"

Article Synopsis
  • cIAPs are proteins that play a crucial role in regulating TNF signaling by modifying RIPK1, and mutations in cIAP1/2 lead to severe embryonic development issues in mice due to apoptosis.
  • While a modified version of RIPK1 can rescue embryonic development, its absence in cIAP1/2 mice results in inflammation and early death after weaning.
  • The study reveals that cIAPs also control TNFR1-mediated toxicity independently of RIPK1 and RIPK3, providing new insights into TNF signaling and creating a mouse model to help evaluate treatments involving TNF inhibitors.
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We report an optofluidic method that enables to efficiently measure the enantiomeric excess of chiral molecules at low concentrations. The approach is to monitor the optical activity induced by a Kagome-lattice hollow-core photonic crystal fiber filled with a sub-μL volume of chiral compounds. The technique also allows monitoring the enzymatic racemization of R-mandelic acid.

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SQSTM1/p62 is a multitasking protein that functions as an autophagy receptor, but also as a signaling hub regulating diverse cellular pathways. p62 accumulation in mice with autophagy-deficient hepatocytes mediates liver damage and hepatocarcinogenesis through Nrf2 overactivation, yet the role of the p62-Keap1-Nrf2 axis in cell death and hepatocarcinogenesis in the absence of underlying autophagy defects is less clear. Here, we addressed the role of p62 and Nrf2 activation in a chronic liver disease model, namely mice with liver parenchymal cell-specific knockout of NEMO (NEMO), in which we demonstrate that they show no inherent autophagy impairment.

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Elevated expression of the X-linked inhibitor of apoptosis protein (XIAP) has been frequently reported in malignant melanoma suggesting that XIAP renders apoptosis resistance and thereby supports melanoma progression. Independent of its anti-apoptotic function, XIAP mediates cellular inflammatory signalling and promotes immunity against bacterial infection. The pro-inflammatory function of XIAP has not yet been considered in cancer.

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The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we assess the impact of mitochondrial bioenergetics on neovascularisation, by deleting cox10 gene encoding an assembly factor of cytochrome c oxidase (COX) specifically in mouse ECs, providing a model for vasculature-restricted respiratory deficiency.

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