A5056310967- Cardiovascular Effects of Exercise
- Osteoarthritis Treatment and Mechanisms
- Skin and Cellular Biology Research
- Cardiomyopathy and Myosin Studies
- Sports injuries and prevention
- COVID-19 Clinical Research Studies
- Glycosylation and Glycoproteins Research
- Plant Reproductive Biology
- Cellular Mechanics and Interactions
- Wnt/β-catenin signaling in development and cancer
- Mesenchymal stem cell research
- Long-Term Effects of COVID-19
- Cardiac electrophysiology and arrhythmias
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Lipid Membrane Structure and Behavior
- Medical and Biological Sciences
- Silk-based biomaterials and applications
- Platelet Disorders and Treatments
- Bacteriophages and microbial interactions
- Knee injuries and reconstruction techniques
- Thermal Regulation in Medicine
- Autoimmune Bullous Skin Diseases
- Bacterial Genetics and Biotechnology
- Proteoglycans and glycosaminoglycans research
- Polyamine Metabolism and Applications
University of Basel
2016-2024
University of Bern
2022-2024
University Hospital of Basel
2015-2019
Wake Forest University
2019
Forest Institute
2019
Charlottesville Medical Research
2019
John Wiley & Sons (United States)
2019
Stockholm University
2013
Arrhythmogenic cardiomyopathy (ACM) is characterized by progressive loss of cardiomyocytes with fibrofatty tissue replacement, systolic dysfunction, and life-threatening arrhythmias. A substantial proportion ACM caused mutations in genes the desmosomal cell-cell adhesion complex, but underlying mechanisms are not well understood. In current study, we investigated relevance defective for development progression.We mutated binding site DSG2 (desmoglein-2), a crucial molecule cardiomyocytes....
As a consequence of SARS-CoV-2 infection various neurocognitive and neuropsychiatric symptoms can appear, which may persist for several months post infection. However, cell type-specific routes brain underlying mechanisms resulting in neuroglial dysfunction are not well understood.
Glycosylation is essential to facilitate cell–cell adhesion and differentiation. We determined the role of dolichol phosphate mannosyltransferase (DPM) complex, a central regulator for glycosylation, desmosomal adhesive function epidermal Deletion key molecule DPM DPM1, in human keratinocytes resulted weakened adhesion, impaired localization components desmoplakin desmoglein-2, led cytoskeletal organization defects keratinocytes. In 3D organotypic epidermis model, loss DPM1 caused...
Abstract Cell-cell junctions, and specifically desmosomes, are crucial for robust intercellular adhesion. Desmosomal function is compromised in the autoimmune blistering skin disease pemphigus vulgaris. We combine whole-genome knockout screening a promotor screen of desmosomal gene desmoglein 3 human keratinocytes to identify novel regulators Kruppel-like-factor 5 (KLF5) directly binds regulatory region promotes Reduced levels KLF5 patient tissue indicate role Autoantibody fractions from...
Most integral membrane proteins, both in prokaryotic and eukaryotic cells, are co-translationally inserted into the via Sec-type translocons: SecYEG complex prokaryotes Sec61 eukaryotes. The contributions of individual amino acids to overall free energy insertion single transmembrane α-helices have been measured for Sec61-mediated endoplasmic reticulum (ER) (Nature 450:1026–1030) but not systematically determined SecYEG-mediated bacterial inner membrane. We now report such measurements,...
Human bone marrow derived mesenchymal stromal cells (BMSCs) represent a putative cell source candidate for tissue engineering-based strategies to repair cartilage and bone. However, traditional isolation of BMSCs by adhesion plastic leads very heterogeneous populations, accounting high variability chondrogenic differentiation outcome, both across donors clonally strains. Identification surface markers able select BMSC subpopulations with higher capacity (CC) reduced variance in could aid the...
Desmoplakin (Dp) is a crucial component of the desmosome, supramolecular cell junction complex anchoring intermediate filaments. The mechanisms how Dp modulates cell-cell adhesion are only partially understood. Here, we studied impact on function desmosomal molecules, desmosome turnover and intercellular adhesion.CRISPR/Cas9 was used for gene editing human keratinocytes which were characterized by Western blot immunostaining. Desmosomal ultrastructure assessed electron microscopy assays....
Intercellular adhesion is essential for tissue integrity and homeostasis. Desmosomes are especially abundant in the epidermis myocardium, tissues, which under constantly changing mechanical stresses. Yet, it largely unclear whether desmosomal can be rapidly adapted to demands mechanisms underlying desmosome turnover only partially understood. We here show that loss of actin-binding protein α-adducin prevented ability cultured keratinocytes or murine withstand stress paralleled with reduced...
ABSTRACT Glycosylation is essential to facilitate cell-cell adhesion and differentiation. We determined the role of dolichol phosphate mannosyltransferase (DPM) complex, a central regulator for glycosylation, desmosomal adhesive function epidermal Deletion key molecule DPM DPM1, in human keratinocytes resulted weakened adhesion, impaired localization components desmoplakin desmoglein-2, led cytoskeletal organization defects keratinocytes. In 3D organotypic epidermis model, loss DPM1 caused...
ABSTRACT Desmoplakin (Dp) localizes to desmosomes, linking clusters of desmosomal adhesion molecules the intermediate filament cytoskeleton. Here, we generated Dp knockout (ko) cell lines human keratinocytes study impact on and desmosome turnover using atomic force microscopy superresolution imaging. In comparison ko another component, plakoglobin (Pg), loss resulted in absence desmosomes drastically impaired cohesion. ko, desmoglein 2 (Dsg2) desmocollin 3 (Dsc3) were redistributed into...
Arrhythmogenic Cardiomyopathy (ACM) in the majority of cases is caused by mutations genes desmosomal cell-cell adhesion complex. ACM characterized progressive loss cardiomyocytes with fibrosis, ventricular systolic dysfunction and life-threatening arrhythmias. Even though pathological phenotype well known, underlying mechanisms are controversial not understood. Here, we tested hypothesis that impaired adhesive function desmosomes central for disease development progression. We generated a...
Abstract Background Arrhythmogenic Cardiomyopathy (ACM) is characterized by progressive loss of cardiomyocytes with fibrofatty replacement, systolic dysfunction and life-threatening arrhythmias. A substantial proportion ACM caused mutations in genes the desmosomal cell-cell adhesion complex, but underlying mechanisms are not well understood. So far, treatment options only symptomatic. Here, we investigate relevance defective for development progression. Methods We mutated binding site...