Research Topics
| Junko KurokawaSummaryAffiliation: Tokyo Medical and Dental University Country: Japan Publications
| Collaborators
|
Detail Information
Publications
Non-genomic action of sex steroid hormones and cardiac repolarizationJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 1 5 45 Yushima, Bunkyo ku, Tokyo 113 8510, Japan
Biol Pharm Bull 36:8-12. 2013..In particular, non-genomic actions of testosterone and progesterone on cardiac ion channels likely to contribute to the gender differences in cardiac repolarization processes...- New aspects for the treatment of cardiac diseases based on the diversity of functional controls on cardiac muscles: acute effects of female hormones on cardiac ion channels and cardiac repolarizationJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
J Pharmacol Sci 109:334-40. 2009..These findings may explain the dynamic changes in risk of arrhythmia in women during the menstrual cycle and around delivery, and they provide clues to avoiding potentially lethal arrhythmias associated with QT prolongation... 
KCNE variants reveal a critical role of the beta subunit carboxyl terminus in PKA-dependent regulation of the IKs potassium channelJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
Channels (Austin) 3:16-24. 2009....- Acute effects of oestrogen on the guinea pig and human IKr channels and drug-induced prolongation of cardiac repolarizationJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 2 3 10 Kandasurugadai, Chiyoda ku, Tokyo 101 0062, Japan
J Physiol 586:2961-73. 2008..Our data indicate that E2 acutely affects the hERG channel gating and the E4031-induced QT(C) prolongation, and may provide a novel mechanism for the higher susceptibility to drug-induced arrhythmia in women... - Compartmentalized regulations of ion channels in the heartJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 2 3 10 Kandasurugadai, Chiyoda ku, Tokyo 101 0062, Japan
Biol Pharm Bull 30:2231-7. 2007..In this review, I will discuss molecular mechanisms of compartmentalized regulation of cardiac ion channels via drugs, cAMP and sex hormones... - [Protein modification of cardiac potassium channels and lethal arrhythmias]Junko Kurokawa
Nippon Yakurigaku Zasshi 126:273-9. 2005 - Progesterone regulates cardiac repolarization through a nongenomic pathway: an in vitro patch-clamp and computational modeling studyHiroaki Nakamura
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo, Japan
Circulation 116:2913-22. 2007..Accumulating clinical evidence suggests a role for progesterone; however, the effect of progesterone on cardiac repolarization remains undetermined... 
Redox- and calmodulin-dependent S-nitrosylation of the KCNQ1 channelKen Asada
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 1 5 45 Yushima, Bunkyo ku, Tokyo 113 8510, Japan
J Biol Chem 284:6014-20. 2009....- Regulation of cardiac ion channels via non-genomic action of sex steroid hormones: implication for the gender difference in cardiac arrhythmiasTetsushi Furukawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Japan
Pharmacol Ther 115:106-15. 2007..In addition to transcriptional regulation, non-transcriptional regulation of cardiac ion channels is in part responsible for the gender difference in LQTS risk and its fluctuation during the menstrual cycle in females... - Nontranscriptional regulation of cardiac repolarization currents by testosteroneChang-Xi Bai
Department of Bio-informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Tokyo 101-0062, Japan
Circulation 112:1701-10. 2005..CONCLUSIONS: The nontranscriptional regulation of IKs and I(Ca,L) by testosterone is a novel regulatory mechanism of cardiac repolarization that can potentially contribute to the control of QTc intervals by androgen... - Ginsenoside Re, a main phytosterol of Panax ginseng, activates cardiac potassium channels via a nongenomic pathway of sex hormonesTetsushi Furukawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
Mol Pharmacol 70:1916-24. 2006..Thus, ginsenoside Re acts as a specific agonist for the nongenomic pathway of sex steroid receptors, and NO released from activated eNOS underlies cardiac K(+) channel activation and protection against ischemia-reperfusion injury... - Non-genomic regulation of cardiac ion channels by sex hormonesTetsushi Furukawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Japan
Cardiovasc Hematol Disord Drug Targets 8:245-51. 2008.... - Role of nitric oxide in Ca2+ sensitivity of the slowly activating delayed rectifier K+ current in cardiac myocytesChang-Xi Bai
Department of Bio-informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
Circ Res 96:64-72. 2005.... - A receptor-independent effect of estrone sulfate on the HERG channelShoko Kakusaka
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
J Pharmacol Sci 109:152-6. 2009..The concentration-dependence of estrone 3-sulfate revealed that physiological levels of circulating estrone 3-sulfate can modulate hERG currents to the maximal extent in both women and men at any age... - A genetically encoded bioluminescent indicator for the sodium channel activity in living cellsAsami Kaihara
Medical Research Institute, Tokyo Medical and Dental University, 1 5 45 Yushima, Bunkyo ku, Tokyo 113 8510, Japan
J Am Chem Soc 131:4188-9. 2009..It may also offer a system for monitoring the Na(+) channel activity in living cells, which may be useful in illuminating neuronal activity in vivo... - Role of transient receptor potential vanilloid 2 in LPS-induced cytokine production in macrophagesKenji Yamashiro
Division of Diabetes and Endocrinology, Department of Internal Medicine, Jikei University School of Medicine, 1 5 45 Yushima, Bunkyo ku, Tokyo 113 8510, Japan
Biochem Biophys Res Commun 398:284-9. 2010.... - Potassium channel remodeling in cardiac hypertrophyTetsushi Furukawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Japan
J Mol Cell Cardiol 41:753-61. 2006.... - Effects of an hERG activator, ICA-105574, on electrophysiological properties of canine heartsMahoko Asayama
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Japan
J Pharmacol Sci 121:1-8. 2013..Our data showed that unbound ICA-105574 caused QT shortening in dogs at concentrations comparable to the half maximal effective concentration (EC(50), 0.42 µM) of hERG activation in the patch clamp studies... - A Combined Approach Using Patch-Clamp Study and Computer Simulation Study for Understanding Long QT Syndrome and TdP in WomenTetsushi Furukawa
Department of Bio Informational Pharmacology, Madical Research Institute, Tokyo Medical and Dental University
Curr Cardiol Rev 4:244-50. 2008..A combined biological and computational approach may provide a powerful means to risk stratify TdP risk in women... - T75M-KCNJ2 mutation causing Andersen-Tawil syndrome enhances inward rectification by changing Mg2+ sensitivityYoshinori Tani
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 2 3 10 Kandasurugadai, Chiyoda ku, Tokyo 101 0062, Japan
J Mol Cell Cardiol 43:187-96. 2007..e., increased sensitivity to intracellular Mg2+ and resultant enhancement of inward rectification. The data presented suggest that the mutation may influence clinical features, but it does not directly show this... - High glucose concentrations impair the activation of K+ channels and proteases in undifferentiated THP-1 monocytesHiroshi Asaoka
Department of Geriatrics and Vascular Medicine, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan
J Med Dent Sci 54:97-102. 2007..Suppression of the transient alkalization and activation of proteases may be one of the mechanisms for bacterial killing by phagocytes in diabetic patients... - Neurohormonal regulation of cardiac ion channels in chronic heart failureJunko Kurokawa
Department of Bio Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo ku, Tokyo, Japan
J Cardiovasc Pharmacol 54:98-105. 2009..The aim of this review was to provide an overview of how cardiac ion channels are regulated by hormones known to play a central role in the pathogenesis of CHF... - Phosphorylation of the A-kinase-anchoring protein Yotiao contributes to protein kinase A regulation of a heart potassium channelLei Chen
Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
J Biol Chem 280:31347-52. 2005..These results suggest, for the first time, a critical role for the PKA phosphorylation of an AKAP in the functional regulation of an ion channel protein and postphosphorylation allosteric modulation of the I(Ks) channel by Yotiao... - Requirement of subunit expression for cAMP-mediated regulation of a heart potassium channelJunko Kurokawa
Department of Pharmacology, College of Physicians and Surgeons of Columbia University, 630 West 168th Street, New York, NY 10032, USA
Proc Natl Acad Sci U S A 100:2122-7. 2003..Transduction of protein phosphorylation into physiologically necessary channel function represents a previously uncharacterized role for the KCNE1 auxiliary subunit, which can be disrupted in LQT-5... - Overexpression of beta2-adrenergic receptors cAMP-dependent protein kinase phosphorylates and modulates slow delayed rectifier potassium channels expressed in murine heart: evidence for receptor/channel co-localizationKeith W Dilly
Department of Pharmacology, Center for Molecular Cardiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
J Biol Chem 279:40778-87. 2004..These data indicate intimate association of KCNQ1 and beta2-ARs and that beta2-AR signaling can modulate the function of IKs channels under conditions of increased beta2-AR expression, even in the absence of exogenous beta-AR agonist... - Regulatory actions of the A-kinase anchoring protein Yotiao on a heart potassium channel downstream of PKA phosphorylationJunko Kurokawa
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
Proc Natl Acad Sci U S A 101:16374-8. 2004..These data reveal previously undescribed actions of Yotiao that occur subsequent to channel phosphorylation and provide evidence that this adaptor protein also may serve as an effector in regulating this important ion channel... - Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channelSteven O Marx
Department of Pharmacology, Center for Molecular Cardiology, Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
Science 295:496-9. 2002..Yotiao binds to hKCNQ1 by a leucine zipper motif, which is disrupted by an LQTS mutation (hKCNQ1-G589D). Identification of the hKCNQ1 macromolecular complex provides a mechanism for SNS modulation of cardiac APD through IKS... - Electrophysiological consequences of human IKs channel expression in adult murine heartChristine Chiello Tracy
Department of Pharmacology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
Am J Physiol Heart Circ Physiol 284:H168-75. 2003..I(Ks) channels impart beta-adrenergic sensitivity to the ventricles and may be responsible for ventricular tachyarrhythmias... - K+ channel structure-activity relationships and mechanisms of drug-induced QT prolongationColleen E Clancy
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
Annu Rev Pharmacol Toxicol 43:441-61. 2003..Drug-induced disruption of cellular repolarization underlies electrocardiographic abnormalities that are diagnostic indicators of arrhythmia susceptibility... - Clinical, genetic, and electrophysiologic characteristics of a new PAS-domain HERG mutation (M124R) causing Long QT syndromeLiat Shushi
Department of Genetics, The Life Sciences Institute, The Hebrew University, Jerusalem, Israel
Ann Noninvasive Electrocardiol 10:334-41. 2005..This mutation markedly decreased the tail-current density and accelerated the deactivation kinetics of the HERG channel in transfected CHO cells...