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Rémi Peyronnet

Researcher at University of Freiburg

Publications -  55
Citations -  1787

Rémi Peyronnet is an academic researcher from University of Freiburg. The author has contributed to research in topics: Medicine & Mechanotransduction. The author has an hindex of 19, co-authored 45 publications receiving 1326 citations. Previous affiliations of Rémi Peyronnet include Imperial College London & University of Nice Sophia Antipolis.

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Two MscS Homologs Provide Mechanosensitive Channel Activities in the Arabidopsis Root

TL;DR: This work uses a combined genetic and electrophysiological approach to show that MSL9 and MSL10, along with three other members of the MSL family, are required for MS channel activities detected in protoplasts derived from root cells, the first molecular identification and characterization of MS channels in plant membranes.
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Piezo1 in Smooth Muscle Cells Is Involved in Hypertension-Dependent Arterial Remodeling

TL;DR: It is shown that Piezo1 is highly expressed in myocytes of small-diameter arteries and that smooth-muscle-specific Piezo 1 deletion fully impairs SAC activity, establishing the connection between an early mechanosensitive process, involvingPiezo1 in smooth muscle cells, and a clinically relevant arterial remodeling.
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Cardiac Mechano-Gated Ion Channels and Arrhythmias

TL;DR: This review focuses on acute mechanical effects on cardiac electrophysiology, explores molecular candidates underlying observed responses, and discusses their pharmaceutical regulation.
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Multiple modalities converge on a common gate to control K2P channel function.

TL;DR: A unique gating mechanism shared by K2P family members is defined and it is suggested that their diverse sensory properties are achieved by coupling different molecular sensors to a conserved core gating apparatus.
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Piezo1-dependent stretch-activated channels are inhibited by Polycystin-2 in renal tubular epithelial cells.

TL;DR: Findings indicate that renal SACs depend on Piezo1, but are critically conditioned by PC2, and PC2 coimmunoprecipitates withPiezo1 and deletion of its N‐terminal domain prevents both this interaction and inhibition of SAC activity.