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Naoki Yahagi

Bio: Naoki Yahagi is an academic researcher from Kyoto University. The author has contributed to research in topics: Sodium channel & Gene expression. The author has an hindex of 2, co-authored 2 publications receiving 1308 citations.

Papers
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Journal ArticleDOI
22 Jun 1989-Nature
TL;DR: Evidence is provided that the positive charges in segment S4 are involved in the voltage–sensing mechanism for activation of the channel and that the region between repeats III and IV is important for its inactivation.
Abstract: Structure-function relationships of the sodium channel expressed in Xenopus oocytes have been investigated by the combined use of site-directed mutagenesis and patch-clamp recording. This study provides evidence that the positive charges in segment S4 are involved in the voltage-sensing mechanism for activation of the channel and that the region between repeats III and IV is important for its inactivation.

1,170 citations

Journal ArticleDOI
TL;DR: MRNA synthesized by transcription in vitro of the cloned cDNA encoding rat brain sodium channel III directs the formation of a functional sodium channel in Xenopus oocytes.

155 citations


Cited by
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Book ChapterDOI
01 Jan 1996
TL;DR: The action potential is triggered when the membrane potential, which was at the resting level, depolarizes and reaches the threshold of excitation, which triggers the action potential.
Abstract: Excitability. Excitability of cell membranes is crucial for signaling in many types of cell. Excitation in the physiological sense means that the cell membrane potential undergoes characteristic changes which, in most cases, go in the depolarizing direction. Single depolarization from the resting potential to potentials near 0 mV has generally been called an action potential. A schematic representation of a neuronal action potential is given in Fig. 12.1 A. The action potential is triggered when the membrane potential, which was at the resting level, depolarizes and reaches the threshold of excitation. This depolarization, which triggers the action potential, is generated by depolarizing synaptic currents, or depolarizing current coming from a membrane region that is already excited (propagation of an action potential), or by pacemaker currents mediated by pacemaker channels, or by current injected externally by an electrode. The duration of different types of action potential varies from seconds to less than 1 ms.

3,016 citations

Journal ArticleDOI
01 Apr 2000-Neuron
TL;DR: Together, these studies showed that the mechanisms of sodium channel function and regulation, purified sodium channel protein contained the essential and gives a perspective for future research on the ex-elements for ion conduction and voltage-dependent panding family of Sodium channel proteins.

2,022 citations

Journal ArticleDOI
19 Mar 1998-Nature
TL;DR: It is shown that sodium channels with the missense mutation recover from inactivation more rapidly than normal and that the frameshift mutation causes the sodium channel to be non-functional.
Abstract: Ventricular fibrillation causes more than 300,000 sudden deaths each year in the USA alone. In approximately 5-12% of these cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation (IVF). A distinct group of IVF patients has been found to present with a characteristic electrocardiographic pattern. Because of the small size of most pedigrees and the high incidence of sudden death, however, molecular genetic studies of IVF have not yet been done. Because IVF causes cardiac rhythm disturbance, we investigated whether malfunction of ion channels could cause the disorder by studying mutations in the cardiac sodium channel gene SCN5A. We have now identified a missense mutation, a splice-donor mutation, and a frameshift mutation in the coding region of SCN5A in three IVF families. We show that sodium channels with the missense mutation recover from inactivation more rapidly than normal and that the frameshift mutation causes the sodium channel to be non-functional. Our results indicate that mutations in cardiac ion-channel genes contribute to the risk of developing IVF.

1,717 citations

Journal ArticleDOI
10 Mar 1995-Cell
TL;DR: Genetic linkage between LQT3 and polymorphisms within SCN5A, the cardiac sodium channel gene, and single strand conformation polymorphism and DNA sequence analyses suggest that mutations in SCN 5A cause chromosome 3-linked LQt and indicate a likely cellular mechanism for this disorder.

1,550 citations

Journal ArticleDOI
26 Oct 1990-Science
TL;DR: A region near the amino terminus with an important role in inactivation has been identified and the results suggest a model where this region forms a cytoplasmic domain that interacts with the open channel to cause inactivation.
Abstract: The potassium channels encoded by the Drosophila Shaker gene activate and inactivate rapidly when the membrane potential becomes more positive. Site-directed mutagenesis and single-channel patch-clamp recording were used to explore the molecular transitions that underlie inactivation in Shaker potassium channels expressed in Xenopus oocytes. A region near the amino terminus with an important role in inactivation has now been identified. The results suggest a model where this region forms a cytoplasmic domain that interacts with the open channel to cause inactivation.

1,511 citations