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Ryuji Inoue

Researcher at Fukuoka University

Publications -  145
Citations -  6896

Ryuji Inoue is an academic researcher from Fukuoka University. The author has contributed to research in topics: Transient receptor potential channel & TRPC6. The author has an hindex of 38, co-authored 141 publications receiving 6442 citations. Previous affiliations of Ryuji Inoue include Kyushu University.

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The Transient Receptor Potential Protein Homologue TRP6 Is the Essential Component of Vascular α1-Adrenoceptor–Activated Ca2+-Permeable Cation Channel

TL;DR: It is found that heterologous expression of murine TRP6 in HEK293 cells reproduces almost exactly the essential biophysical and pharmacological properties of &agr;1-adrenoceptor–activated nonselective cation channels (&agr–1-AR–NSCC) previously identified in rabbit portal vein smooth muscle.
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Nitric oxide activates TRP channels by cysteine S-nitrosylation

TL;DR: Findings reveal the structural motif for the NO-sensitive activation gate in TRP channels and indicate that NO sensors are a new functional category of cellular receptors extending over different TRP families.
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Molecular and Functional Characterization of a Novel Mouse Transient Receptor Potential Protein Homologue TRP7 Ca2+-PERMEABLE CATION CHANNEL THAT IS CONSTITUTIVELY ACTIVATED AND ENHANCED BY STIMULATION OF G PROTEIN-COUPLED RECEPTOR

TL;DR: These findings reveal an interesting correspondence of TRP7 to the background and receptor stimulation-induced cation currents in various native systems and suggest that the TRP6 channel is a new member of diacylglycerol-activated cation channels.
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TRPC3 and TRPC6 are essential for angiotensin II-induced cardiac hypertrophy.

TL;DR: Data suggest that DAG‐induced Ca2+ signaling pathway through TRPC3 and TRPC6 is essential for Ang II‐induced NFAT activation and cardiac hypertrophy.
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Transient Receptor Potential Channels in Cardiovascular Function and Disease

TL;DR: An overview of the current knowledge on TRP proteins is provided and new lines of evidence suggest that TRPV2 may act as a Ca2+-overloading pathway associated with dystrophic cardiomyopathy,TRPV4 as a mediator of endothelium-dependent hyperpolarization, TRPM7 as a proproliferative vascular Mg2+ entry channel, and TRPP2 as aCa2-entry channel requisite for vascular integrity.