Inanobe Atsushi

イナノベアツシ | Inanobe Atsushi

Affiliation and department：

Research field (1)： Pharmacology

Research keywords (4)：薬理学 , 神経生理学 , 構造生物学 , 電気生理学

Research theme for competitive and other funds (24)：

2022 - 2025 心房細動治療を目指した革新的な作用機序を示す薬物の開発
2017 - 2020 Mathematical analysis of arrhythmogenesis for bradycardia
2010 - 2016 Research and development of a software platform for integrative multi-level systems biology
2011 - 2013 Molecular basis for the cation-chloride co-transporter activity
2008 - 2010 Studies on the structure-activity relationship on pharmacological modulations of potassium channels

2005 - 2009 Physiological regulation of G protein signaling by RGS proteins

2007 - 2008 Structural basis of the calcium-dependent modulation of G protein signaling

2007 - 2008 カルシウムによるイオンチャネル活性調節の構造的基盤の解析

2003 - 2005 Molecular mechanisms for functional and spatial regulation of the G protein-gated potassium channel

2000 - 2005 The physiological roles and molecular basis of polarized localization of K+ channels in the vectorial transports of ions and water.

2001 - 2002 カリウムチャネルのシナプス局在と膜電位調節の分子基盤の解明

1999 - 2000 黒質ドーパミン神経のG蛋白質制御内向き整流カリウムチャネルによる機能制御機構

1999 - 2000 Regulation of cardio-vascular ATP-sensitive K channels.

1998 - 2000 ATP感受性カリウムチャネルの分子制御機構と生理作用

1998 - 1999 Molecular dissection of inwardly rectifying KィイD1+ィエD1 channel, Kir4.1/KィイD2abィエD2-2, of glial cells.

1998 - 1998 G蛋白質制御カリウムチャネルと神経伝達

1997 - 1998 Investigation of Molecular Diversity of ATP-Sensitive K^+ Channels.

1997 - 1998 Its functional significance and molecular mechanism

1996 - 1998 Studies of inwardly rectifying K^+ channels and an approach to develop new methods for assaying K^+ channel activity.

1995 - 1998 Molecular Mechanism in Regulation of Inwardly Rectifying Potassium Channel and its Functional Disorder

1996 - 1997 Analysis of the polyamine-binding sites in inwardly rectifying K^+ channels.

1995 - 1995 三量体GTP結合蛋白質とムスカリン性K^+チャネルの相互作用の解析

内向き整流性カリウムチャネルの生化学的解析

Biochemical characterization of inwardly rectifying potassium channels

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Papers (79)：

山田憲明, 朝野仁裕, 稲野辺厚, 石綿紀久, 倉智嘉久, 北風政史, 坂田泰史, 高島成二. 徐脈性不整脈の薬理学的標的としての機能獲得型変異体IKAChチャネル(Gain-of-function Mutant IKACh Channels as a Pharmacological Target for Bradyarrhythmia). 日本循環器学会学術集会抄録集. 2020. 84回. OJ31-6
山田憲明, 朝野仁裕, 稲野辺厚, 石綿紀久, 倉智嘉久, 北風政史, 坂田泰史, 高島成二. Gain-of-function Mutant IKACh Channels as a Pharmacological Target for Bradyarrhythmia(和訳中). 日本循環器学会学術集会抄録集. 2020. 84回. OJ31-6
Noriaki Yamada, Yoshihiro Asano, Masashi Fujita, Satoru Yamazaki, Atsushi Inanobe, Norio Matsuura, Hatasu Kobayashi, Seiko Ohno, Yusuke Ebana, Osamu Tsukamoto, et al. Mutant KCNJ3 and KCNJ5 Potassium Channels as Novel Molecular Targets in Bradyarrhythmias and Atrial Fibrillation. Circulation. 2019. 139. 18. 2157-2169
Inanobe A, Itamochi H, Kurachi Y. Kir Channel Blockages by Proflavine Derivatives via Multiple Modes of Interaction. Molecular pharmacology. 2018. 93. 6. 592-600
Masato Kinboshi, Takahiro Mukai, Yuki Nagao, Yusuke Matsuba, Yoshimi Tsuji, Shiho Tanaka, Kentaro Tokudome, Saki Shimizu, Hidefumi Ito, Akio Ikeda, et al. Inhibition of Inwardly Rectifying Potassium (Kir) 4.1 Channels Facilitates Brain-Derived Neurotrophic Factor (BDNF) Expression in Astrocytes. FRONTIERS IN MOLECULAR NEUROSCIENCE. 2017. 10. 408

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MISC (57)：

A. Inanobe, C. Tsuzuki, Y. Kurachi. CALML3 IS A CONSTITUENT OF FUNCTIONAL KCNQ1 CHANNELS IN THE EPITHELIUM. BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY. 2014. 115. 256-257
Inanobe Atsushi, Nakagawa Atsushi, Kurachi Yoshihisa. Structural Elements in the Cytoplasmic Domain of Mammalian Inward Rectifier K+ Channels Responsible for Gating. Biophysical Journal. 2013. 104. 2. 624P
Inanobe Atsushi, Nakagawa Atsushi, Kurachi Yoshihisa. Domain Coupling in Inward Rectifier Potassium Channels. Journal of Pharmacological Sciences. 2013. 121. 86P
Shingo Murakami, Atsushi Inanobe, Yoshihisa Kurachi. Simulation analysis of short-term desensitization of muscarinic K+ current in the heart. JOURNAL OF PHARMACOLOGICAL SCIENCES. 2013. 121. 166P-166P
Atsushi Inanobe, Chizuru Tsuzuki, Yoshihisa Kurachi. Classification of long-QT syndrome type-1 mutations by the ability to bind calmodulin. JOURNAL OF PHYSIOLOGICAL SCIENCES. 2013. 63. S245-S245

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Education (3)：

1991 - 1994 Tokyo Institute of Technology Interdisciplinary Science and Engineering
1989 - 1991 Tokyo Institute of Technology Interdisciplinary Science and Engineering
1985 - 1989 Tohoku University Faculty of Science

Professional career (1)：

Work history (4)：

Association Membership(s) (5)：

米国生物物理学会 , 日本神経科学会 , 日本生化学会 , 日本薬理学会 , Biophysical Society

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