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Keiji Imoto

Researcher at Graduate University for Advanced Studies

Publications -  115
Citations -  15331

Keiji Imoto is an academic researcher from Graduate University for Advanced Studies. The author has contributed to research in topics: Neurotransmission & Voltage-dependent calcium channel. The author has an hindex of 51, co-authored 114 publications receiving 14628 citations. Previous affiliations of Keiji Imoto include Colorado State University & Shizuoka University.

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A high signal-to-noise Ca(2+) probe composed of a single green fluorescent protein.

TL;DR: G-CaMP will be a useful tool for visualizing intracellular Ca2+ in living cells and Mutational analysis, together with previous structural information, suggests the residues that may alter the fluorescence of GFP.
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Molecular distinction between fetal and adult forms of muscle acetylcholine receptor

TL;DR: The conductance and gating properties of the two classes of channels suggest that replacement of the γ-subunit by the ε- subunit is responsible for the functional alteration of the receptor during muscle development.
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Primary structure and functional expression of the cardiac dihydropyridine-sensitive calcium channel

TL;DR: It is shown that messenger RNA derived from the cardiac DHP receptor cDNA is sufficient to direct the formation of a functional DHP-sensitive calcium channel in Xenopus oocytes, and higher calcium-channel activity is observed when mRNA specific for the polypeptide of relative molecular mass associated with the skeletal muscle DHP receptors is co-injected.
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Primary structure and functional expression from complementary dna of a brain calcium channel

TL;DR: The primary structure of a voltage-dependent cal-cium channel from rabbit brain has been deduced by cloning and sequencing the complementary DNA and it is suggested that it is expressed predominantly in cerebellar Purkinje cells and granule cells.
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LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death

TL;DR: It is reported that a widely expressed Ca2+-permeable cation channel, LTRPC2, activated by micromolar levels of H2O2 and agents that produce reactive oxygen/nitrogen species represents an important intrinsic mechanism that mediatesCa2+ and Na+ overload in response to disturbance of redox state in cell death.