K
Ken-ichi Amano
Researcher at University of Tokyo
Publications - 7
Citations - 837
Ken-ichi Amano is an academic researcher from University of Tokyo. The author has contributed to research in topics: Thapsigargin & Phylogenetic tree. The author has an hindex of 4, co-authored 6 publications receiving 826 citations.
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Journal Article
Calcium Movements, Distribution, and Functions in Smooth Muscle
Hideaki Karaki,Hiroshi Ozaki,Masatoshi Hori,Minori Mitsui-Saito,Ken-ichi Amano,Ken-ichi Harada,Shigeki Miyamoto,Hiroshi Nakazawa,Kyung-Jong Won,Koichi Sato +9 more
TL;DR: Contraction of smooth muscle is regulated by the cytosolic Ca2+ level ([Ca2+]i)b, and the sensitivity of the contractile elements in response to changes in the environment surrounding the cell.
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Membrane permeabilization induced by discodermin A, a novel marine bioactive peptide.
Koichi Sato,Kikuko Horibe,Ken-ichi Amano,Minori Mitusi-Saito,Masatoshi Hori,Shigeki Matsunaga,Nobuhiro Fusetani,Hiroshi Ozaki,Hideaki Karaki +8 more
TL;DR: Results suggest that DC-A has a permeabilizing effect on the plasma membrane possibly by interacting with plasma membrane phospholipids with its six successive hydrophobic amino acid residues at N-terminal.
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Palytoxin-induced increase in endothelial Ca2+ concentration in the rabbit aortic valve
TL;DR: It is suggested that PTX increases [Ca2+]i in the endothelium of the rabbit aortic valve by increasing Ca2+ influx through a pathway which is different from that activated by ATP or thapsigargin.
Journal Article
Ca++ mobilization mediated by endothelin ETA receptor in endothelium of rabbit aortic valve.
TL;DR: The results suggest that, in the endothelium of rabbit aortic valve, only the ETA receptor mediates the effects of ETs to increase [Ca++]i, which is attributable to the release of Ca++ from thapsigargin-sensitive and ryanodine-insensitive Ca++ stores and also to the Ca++ influx through La (-)sensitive and dihydropyridine-inssensitive Ca++ channels.
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Agonist-dependent difference in the relationship between cytosolic Ca2+ level and release of vascular relaxing factors in the endothelium of rabbit aortic valve.
TL;DR: The results suggest that the endothelial relaxing factors released from aortic valve are nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), and various agonists differently modulate the relationship between [Ca2+]i and release of NO.