Marc Freichel

Canonical transient receptor channel 5 (TRPC5) and TRPC1/4 contribute to seizure and excitotoxicity by distinct cellular mechanisms.

The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone.

TRPC4- and TRPC4-containing channels.

Adenylyl cyclase-mediated effects contribute to increased Isoprenaline-induced cardiac contractility in TRPM4-deficient mice.

A background Ca2+ entry pathway mediated by TRPC1/TRPC4 is critical for development of pathological cardiac remodelling.

TRPM4-mediated control of FcεRI-evoked Ca(2+) elevation comprises enhanced plasmalemmal trafficking of TRPM4 channels in connective tissue type mast cells.

Dicarbonyls and Advanced Glycation End-Products in the Development of Diabetic Complications and Targets for Intervention.

Heteromeric channels formed by TRPC1, TRPC4 and TRPC5 define hippocampal synaptic transmission and working memory.

TRPC proteins contribute to development of diabetic retinopathy and regulate glyoxalase 1 activity and methylglyoxal accumulation.

Deletion of Orai2 augments endogenous CRAC currents and degranulation in mast cells leading to enhanced anaphylaxis.

Compensatory mechanisms for methylglyoxal detoxification in experimental & clinical diabetes.

Methylglyoxal evokes acute Ca transients in distinct cell types and increases agonist-evoked Ca entry in endothelial cells via CRAC channels.

Assessment of PEEP-Ventilation and the Time Point of Parallel-Conductance Determination for Pressure-Volume Analysis Under β-Adrenergic Stimulation in Mice.

Angiotensin-II-Evoked Ca Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels.

Analysis of Mrgprb2 Receptor-Evoked Ca Signaling in Bone Marrow Derived (BMMC) and Peritoneal (PMC) Mast Cells of TRPC-Deficient Mice.

Cardiomyocyte-Specific Deletion of Orai1 Reveals Its Protective Role in Angiotensin-II-Induced Pathological Cardiac Remodeling.

Transcriptional signatures regulated by TRPC1/C4-mediated Background Ca entry after pressure-overload induced cardiac remodelling.

L-type blocker STIMulate Ca entry in synthetic VSMCs.

Control of Insulin Release by Transient Receptor Potential Melastatin 3 (TRPM3) Ion Channels.

Genetic background influences expression and function of the cation channel TRPM4 in the mouse heart.

Development of an AAV9-RNAi-mediated silencing strategy to abrogate TRPM4 expression in the adult heart.