Area of research
Molecular Biology · Immunology
Research interest
Research interests include Redox biology and oxidative stress, Neutrophil, Myeloperoxidase and Oxidative Mechanisms, Electron Spin Resonance Studies, and Nitric Oxide and Endothelin Effects.
Proteomics and ex vivo plaque culture identify the insulin-like growth factor axis as a potential regulator of matrix remodelling in carotid plaques.
Alexander disease mutations differentially sensitize glial fibrillary acidic protein (GFAP) to posttranslational modifications and network disruption by oxidants.
Nitrated products formed on α-synuclein are preferentially incorporated into oligomers but excluded from fibrils: A mechanism for accumulation of neurotoxic species.
Elevated Asporin expression in human atherosclerotic plaques promotes their stability and reduces the risk for cardiovascular events.
Methionine oxidation products as biomarkers of oxidative damage to proteins and modulators of cellular metabolism and toxicity
Unravelling molecular mechanisms in atherosclerosis using cellular models and omics technologies.
N-Terminal Proteomics Reveals Distinct Protein Degradation Patterns in Different Types of Human Atherosclerotic Plaques.
Current status and challenges of multi-omics research using animal models of atherosclerosis.
Hypoxia promotes the generation of a versican-rich extracellular matrix by human coronary artery endothelial cells.
Dimethyl labeling of N-terminal amines allows unambiguous identification of protein crosslinks.
Parthenolide disrupts mitosis by inhibiting ZNF207/BUGZ-promoted kinetochore-microtubule attachment.
Spatial proteomics of the human atherosclerotic microenvironment reveals heterogeneity in intra-plaque proteomes and extracellular matrix remodeling
Quantitative analysis of the proteome and protein oxidative modifications in primary human coronary artery endothelial cells and associated extracellular matrix.
Inactivation of human glucose 6-phosphate dehydrogenase (G6PDH) by peroxyl radicals is strongly modulated by its substrate and cofactor.
Iodide influences the sensitized one-electron photo-oxidation of Tyr and Trp residues by competition reaction
Isoform-specific oxidative modifications of tropoelastin by HOCl and MPO alter protein self-assembly.
Oxidation products of proteins in plasma of newborns reflect damage inflicted by O<sub>2</sub> supplementation and correlate with gestational age.
Peroxidase-Catalyzed and Photo-Oxidation of Tryptophan Results in Distinct Isomeric Tryptophan Dimers.
Inactivation of mitochondrial pyruvate dehydrogenase by singlet oxygen involves lipoic acid oxidation, side-chain modification and structural changes.
Sacrificial redox modulation by a secreted bacterial effector molecule mitigates oxidative stress and inflammation in vivo.
Peptidomic and proteomic analysis of precision-cut lung slice supernatants.
Proteomic analysis of the extracellular matrix of human atherosclerotic plaques shows marked changes between plaque types.
Elevated levels of iodide promote peroxidase-mediated protein iodination and inhibit protein chlorination
Modification of extracellular matrix proteins by oxidants and electrophiles.
Oxidation of the active site cysteine residue of glyceraldehyde-3-phosphate dehydrogenase to the hyper-oxidized sulfonic acid form is favored under crowded conditions.
Competitive oxidation of key pentose phosphate pathway enzymes modulates the fate of intermediates and NAPDH production.
Elevated levels of iodide promote peroxidase-mediated protein iodination and inhibit protein chlorination.
Selenocyanate (SeCN−) acts as an efficient competitive substrate for myeloperoxidase and decreases biological damage induced by hypochlorous acid
Protein nitration in the artery wall: A contributor to cardiovascular disease?
Macromolecular crowding and bicarbonate enhance the hydrogen peroxide-induced inactivation of glyceraldehyde-3-phosphate dehydrogenase.