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Alexander Dietrich

Researcher at Ludwig Maximilian University of Munich

Publications -  132
Citations -  8613

Alexander Dietrich is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Transient receptor potential channel & TRPC. The author has an hindex of 49, co-authored 120 publications receiving 7689 citations. Previous affiliations of Alexander Dietrich include University of Ulm & University of Marburg.

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Evidence for a supportive role of classical transient receptor potential 6 (TRPC6) in the exploration behavior of mice.

TL;DR: Most interestingly, TRPC6(-/-) mice showed no significant differences in anxiety in a marble-burying test, but demonstrated reduced exploration in the square open field and the elevated star maze, suggesting that TRPC 6 channel activity may play a yet unknown role for exploration behavior.
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Identification of a three-amino-acid region in G protein gamma 1 as a determinant of selective beta gamma heterodimerization.

TL;DR: The results of this study argue against the notion that the hydrophobic terminal residue of this motif represents the key determinant of selective beta gamma interaction.
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Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

TL;DR: The dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs is concluded and the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca 2+ entry pathway is suggested.
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Hypoxic pulmonary vasoconstriction in isolated mouse pulmonary arterial vessels.

TL;DR: It is found that only small intrapulmonary arteries (80–200 μm in diameter) exhibit hypoxic pulmonary vasoconstriction, and the observed response was sustained, significantly potentiated by depolarization‐induced preconstriction and not dependent on the endothelium or TRPC6 channels.
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TRPA1 channels: expression in non-neuronal murine lung tissues and dispensability for hyperoxia-induced alveolar epithelial hyperplasia

TL;DR: TRPA1 expression does neither appear to be a key player for hyperoxia-induced changes in [Ca2+]i levels in primary lung epithelial cells, nor being essential for the development of hyperoxIA-induced alveolar epithelial hyperplasia.