Saito Hirohide | Department Of Gene Mechanisms Graduate School Of Biostudies Kyoto University
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概要
- Saito Hirohideの詳細を見る
- 同名の論文著者
- Department Of Gene Mechanisms Graduate School Of Biostudies Kyoto Universityの論文著者
関連著者
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SAITO Hirohide
Department of Protein Engineering, Cancer Institute, Japanese Foundation for Cancer Research
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Saito Hirohide
Department Of Gene Mechanisms Graduate School Of Biostudies Kyoto University
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YAMORI Takao
Division of Molecular Pharmacology, Cancer Chemotherapy Center, Japanese Foundation for Cancer Resea
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INOUE Tan
Department of Chemistry. Faculty of Science, Kyoto niversity
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Yamori Takao
Division Of Experimental Chemotherapy Cancer Chemotherapy Center Japanese Foundation For Cancer
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SHIBA Kiyotaka
Department of Protein Engineering Cancer Institute, Japanese Foundation for Cancer Research
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Shiba Kiyotaka
Department Of Protein Engineering Cancer Institute Japanese Foundation For Cancer Research
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Inoue Tan
Department Of Gene Mechanisms Graduate School Of Biostudies Kyoto University
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MINAMISAWA Tamiko
Department of Protein Engineering, Cancer Institute, Japanese Foundation for Cancer Research
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Yamori Takao
Division Of Molecular Pharmacology Cancer Chemotherapy Center Japanese Foundation For Cancer Researc
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Kitamura Aya
ICORP, Japan Science and Technology Corporation (JST)
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Westhof Eric
Institut de Biologie Moleculaire et Cellulaire, CNRS
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Westhof Eric
Institut De Biologie Moleculaire Et Cellulaire Cnrs
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Kitamura Aya
Icorp Japan Science And Technology Corporation (jst)
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Saito Hirohide
Department Of Protein Engineering Cancer Institute Japanese Foundation For Cancer Research
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Minamisawa Tamiko
Department Of Protein Engineering Cancer Institute Japanese Foundation For Cancer Research
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Shiba Kiyotaka
Department of Protein Engineering, Cancer Institute, Japanese Foundation for Cancer Research
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Inoue Tan
Department of Chemistry, Tokyo Institute of Technology
著作論文
- 3P-233 RNA-タンパク質相互作用の共変化の,kink-turn motifにおける相互情報量計算による同定(生命情報科学-分子進化,第47回日本生物物理学会年会)
- Motif-programmed artificial protein induces apoptosis in several cancer cells by disrupting mitochondria