首页> Biochemical pharmacology> Distinct mechanisms of cell-kill by triapine and its terminally dimethylated derivative Dp44mT due to a loss or gain of activity of their copper(II) complexes.

Distinct mechanisms of cell-kill by triapine and its terminally dimethylated derivative Dp44mT due to a loss or gain of activity of their copper(II) complexes.

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第一作者： Kimiko,Ishiguro

第一单位： Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: kimiko.ishiguro@yale.edu.

作者： Kimiko,Ishiguro ^[1] ; Z Ping,Lin ^[2] ; Philip G,Penketh ^[2] ; Krishnamurthy,Shyam ^[2] ; Rui,Zhu ^[2] ; Raymond P,Baumann ^[2] ; Yong-Lian,Zhu ^[2] ; Alan C,Sartorelli ^[2] ; Thomas J,Rutherford ^[3] ; Elena S,Ratner ^[4]

作者单位： Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: kimiko.ishiguro@yale.edu. ^[1] Department of Pharmacology and Developmental Therapeutics Program, Yale Cancer Center, Yale University School of Medicine, New Haven, CT 06520, United States. ^[2] Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Yale University School of Medicine, New Haven, CT 06520, United States. ^[3] Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: elena.ratner@yale.edu. ^[4]

关键词 DNA double-strand breaks DNA replication stress Dp44mT (di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone)Metal coordination Reactive oxygen species Triapine (3-AP, 3-aminopyridine-2-carboxaldehyde thiosemicarbazone)