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How to find us prof. dr. M. (Martina) Schmidt

Research interests

My research focus on clustered signaling pathways of molecular partners in defined subcellular compartments (signalosomes) that enables cells to exert highly specialized tasks. Actually, our goal for the future is to unravel the organization of the recently discovered signaling components within functional units by biochemical, molecular, cell biological methods, genetic and omic’s. Research is embedded in the field of integrative pharmacology and translational medicine. We have directed our attention to chronic inflammatory disorders, as evidence exist for a role of our signaling components (Epac, PLD, AKAP, cofilin) in smooth muscle cells, neuronal cells, immune cells as well as cardiomyocytes. Many devastating diseases, e.g. cancer, type-II diabetes mellitus, Alzheimers’s dementia, cardiovascular and airway diseases (heart failure, cardiac arrhythmia, developmental defects, asthma and COPD), and infection diseases are associated with defective or derailed signaling processes, and research into the control of these processes clearly is of great public and social importance as well. My research group integrates in vivo, ex vivo translational pharmacology, molecular (cell) biology. Novel techniques like microfluidics, precision cut lung slices and others.



Elevated cAMP protects against diclofenac-induced toxicity in primary rat hepatocytes: a protective effect mediated by EPACs

A-Kinase Anchoring Proteins Diminish TGF-β1/Cigarette Smoke-Induced Epithelial-To-Mesenchymal Transition

Cigarette smoke exposure alters phosphodiesterases in human structural lung cells

Diesel exhaust particles alter mitochondrial bioenergetics in human bronchial epithelial cells

Diesel Exhaust Particles-induced Dysfunctional Responses in Lung Epithelial Progenitors is mediated by oxidative stress

Diesel Exhaust Particles-induced Dysfunctional Responses in Lung Epithelial Progenitors is mediated by oxidative stress

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Disruption of AKAP-PKA Interaction Induces Hypercontractility With Concomitant Increase in Proliferation Markers in Human Airway Smooth Muscle

Involvement of NDPK-B in Glucose Metabolism-Mediated Endothelial Damage via Activation of the Hexosamine Biosynthesis Pathway and Suppression of O-GlcNAcase Activity

Metformin protects against diclofenac - induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via an alternative pathway involving epac

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