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Katsutoshi Goto

Researcher at University of Tsukuba

Publications -  231
Citations -  31742

Katsutoshi Goto is an academic researcher from University of Tsukuba. The author has contributed to research in topics: Endothelin 1 & Endothelin receptor. The author has an hindex of 63, co-authored 228 publications receiving 31015 citations. Previous affiliations of Katsutoshi Goto include University of Texas Southwestern Medical Center.

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Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT1A Receptor

TL;DR: 5-HT hyperpolarizes orexin neurons through the 5-HT1A receptor and subsequent activation of the GIRK and that this inhibitory serotonergic input to the orexIn neurons is likely to be important for the physiological regulation of this neuropeptide system.
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Conversion of big endothelin-1 to 21-residue endothelin-1 is essential for expression of full vasoconstrictor activity: structure-activity relationships of big endothelin-1.

TL;DR: Results indicate that the conversion of bigET-1 to “mature” ET-1 is essential for the expression of the full vasoconstrictor activity, suggesting the physiological importance of the unusual proteolytic processing catalyzed by the putative “ET converting enzyme.”
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Endothelin receptor is coupled to phospholipase C via a pertussis toxin-insensitive guanine nucleotide-binding regulatory protein in vascular smooth muscle cells.

TL;DR: Results indicate that the receptor for ET is coupled to phospholipase C via a guanine nucleotide-binding regulatory protein which is distinct from the pertussis toxin substrate in A-10 cells.
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Orexin receptor type-1 couples exclusively to pertussis toxin-insensitive G-proteins, while orexin receptor type-2 couples to both pertussis toxin-sensitive and -insensitive G-proteins.

TL;DR: It is found that a phospholipase C (PLC)-inhibitor, U73122, inhibits orexin-mediated neuronal activation, but PTX showed no effect on it, which suggests that although OX2R couples to multiple G-proteins, activation of neurons by orexins through Ox2R is mediated via a PTX-insensitive, PLC dependent pathway.
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Endothelin acts in feline and canine cerebral arteries from the adventitial side.

TL;DR: The long-lasting nature of endothelin-induced constriction of the cerebral arteries in vivo suggests that the peptide might be involved in the pathogenesis of cerebral vasospasm, possibly due to the presence of the blood-arterial wall barrier.