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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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Journal ArticleDOI
Alkylated epidermal creatine kinase as a biomarker for sulfur mustard exposure: comparison to adducts of albumin and DNA in an in vivo rat study.
Dirk Steinritz,Robin Lüling,Markus Siegert,Julia Herbert,Harald Mückter,Christian D. Taeger,Thomas Gudermann,Alexander Dietrich,Horst Thiermann,Harald John +9 more
TL;DR: In this paper, a novel biomarker, namely creatine kinase (CK) B-type, suitable as a local biomarker for sulfur mustard exposure on the skin was reported.
Journal ArticleDOI
Store-operated Ca 2+ entry in primary murine lung fibroblasts is independent of classical transient receptor potential (TRPC) channels and contributes to cell migration.
TL;DR: It is shown that TRPC1/6 channels are not involved in SOCE and STIM1/2 deficiency resulted in decreased cell proliferation and migration in pmLF, and cell proliferation, migration and nuclear localization of nuclear factor of activated T-cells were decreased.
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TRP channel function in platelet and megakaryocyte: Basic mechanisms and pathophysiological impact.
TL;DR: Transient receptor potential (TRP) proteins form a superfamily of cation channels that are expressed in a wide range of tissues and cell types as mentioned in this paper , and the diversity of functions depends on multiple regulatory mechanisms by which TRP channels regulate Ca2+ entry mechanisms and intracellular Ca 2+ dynamics, either through membrane depolarization involving cation influx or store-and receptor-operated mechanisms.
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Transcriptional signatures regulated by TRPC1/C4-mediated Background Ca2+ entry after pressure-overload induced cardiac remodelling
Juan E. Camacho Londoño,Vladimir Kuryshev,Markus Zorn,Kathrin Saar,Qinghai Tian,Norbert Hubner,Peter P. Nawroth,Alexander Dietrich,Lutz Birnbaumer,Peter Lipp,Christoph Dieterich,Marc Freichel +11 more
TL;DR: Deletion of the TRPC1 and TRPC4 channel proteins protects against development of pathological cardiac hypertrophy independently of the genetic background.
Journal ArticleDOI
TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons.
TL;DR: TRPC1 has an inhibitory effect on receptor-operated nonselective cation channels in hippocampal CA1 neurons probably as a result of heterotetramer formation with other TRPC isoforms, and that TRPC1 deletion has only minor effects on dendritic morphology.