Tomoda Akio | Dep. Of Biochemistry Tokyo Medical Univ. Jpn
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概要
関連著者
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Tomoda Akio
Dep. Of Biochemistry Tokyo Medical Univ. Jpn
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Tomoda Akio
Department Of Biochemistry And Intractable Tokyo Medical University
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Tomoda Akio
Department Of Biochemistry And Intractable Immune System Disease Research Center Tokyo Medical Unive
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Tomoda Akio
Department of Biochemistry and Intractable Immune System Disease Research Center, Tokyo Medical Univ
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SHIRATO Ken
Laboratory of Physiological Sciences, Faculty of Human Sciences, Waseda University
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Shirato Ken
Laboratory Of Physiological Sciences Faculty Of Human Sciences Waseda University
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Shirato Ken
Laboratory Of Physiological Sciences Graduate School Of Human Sciences Waseda University
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IMAIZUMI Kazuhiko
Laboratory of Physiological Sciences, Faculty of Human Sciences, Waseda University
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Tomoda A
Tokyo Medical Univ.
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KUROSAKI Kunihiko
Department of Legal Medicine, School of Medicine, Toho University
著作論文
- Anticancer Effects of Phenoxazine Derivatives Revealed by Inhibition of Cell Growth and Viability, Disregulation of Cell Cycle, and Apoptosis Induction in HTLV-1-Positive Leukemia Cells
- Apoptosis Induction Preceded by Mitochondrial Depolarization in Multiple Myeloma Cell Line U266 by 2-Aminophenoxazine-3-one(Medicinal Chemistry)
- β_2-Agonist Clenbuterol Induced Changes in the Distribution of White Blood Cells in Rats
- Phenoxazine Derivatives 2-Amino-4,4α-dihydro-4α-phenoxazine-3-one and 2-Aminophenoxazine-3-one-Induced Apoptosis through a Caspase-Independent Mechanism in Human Neuroblastoma Cell Line NB-1 Cells(Medicinal Chemistry)
- 2-Aminophenoxazine-3-one Suppresses the Growth of Mouse Malignant Melanoma B16 Cells Transplanted into C57BL/6Cr Slc Mice(Pharmacology)
- 2-Aminophenoxazine-3-one Prevents Pulmonary Metastasis of Mouse B16 Melanoma Cells in Mice
- Selectively Induced Apoptosis in Human Neutrophils in the Presence of Oxidative Phenoxazines, 2-Amino-4,4α-dihydryo-4α-7H-phenoxazine-3-one and 2-Aminophenoxazine-3-one, Preceded by Decrease of Intracellular pH, Depolarization of the Mitochondria, and Inh