A5023277105- Cell death mechanisms and regulation
- PARP inhibition in cancer therapy
- SARS-CoV-2 and COVID-19 Research
- Lipid Membrane Structure and Behavior
- Pancreatic function and diabetes
- Ion channel regulation and function
- Cancer Genomics and Diagnostics
- Electrochemical Analysis and Applications
- Radiation Therapy and Dosimetry
- Retinal and Optic Conditions
- Diabetes and associated disorders
- COVID-19 Clinical Research Studies
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2024
University of Cologne
2024
Champalimaud Foundation
2020
Universidade de São Paulo
1988
Abstract The dysregulated immune response and inflammation resulting in severe COVID-19 are still incompletely understood. Having recently determined that aberrant death-ligand-induced cell death can cause lethal inflammation, we hypothesized this process might also or contribute to inflammatory disease lung failure following SARS-CoV-2 infection. To test hypothesis, developed a novel mouse-adapted model (MA20) recapitulates key pathological features of COVID-19. Concomitantly with...
Abstract Necroptosis is a caspase-independent modality of cell death implicated in many inflammatory pathologies. The execution this pathway requires the formation cytosolic platform that comprises RIPK1 and RIPK3 which, turn, mediates phosphorylation pseudokinase MLKL (S345 mouse). activation executioner followed by its oligomerisation accumulation at plasma-membrane where it leads to via destabilisation consequent permeabilisation. While biochemical cellular characterisation these events...
Receptor-interacting protein kinase 1 (RIPK1) orchestrates the decision between cell survival and death in response to tumor necrosis factor (TNF) other cytokines. Whereas scaffolding function of RIPK1 is crucial prevent TNF-induced apoptosis necroptosis, its activity required for necroptosis partially apoptosis. Although TNF a proinflammatory cytokine associated with β-cell loss diabetes, mechanism by which induces demise remains unclear.
Poly (ADP-ribose) polymerase (PARP) inhibition in BRCA-mutated cells results an incapacity to repair DNA damage, leading cell death caused by synthetic lethality. Within the treatment options for advanced triple negative breast cancer, PARP inhibitor olaparib is only given patients with BRCA1/2 mutations. However, these may show resistance this drug and wild-type tumors can a striking sensitivity, making BRCA status poor biomarker choice. Aiming investigate if zebrafish model discriminate...