Mechanism of the induction of endoplasmic reticulum stress by the anti-cancer agent, di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT): Activation of PERK/eIF2α, IRE1α, ATF6 and calmodulin kinase.

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作者： Angelica M,Merlot ^[1] ; Nurul H,Shafie ^[2] ; Yu,Yu ^[1] ; Vera,Richardson ^[1] ; Patric J,Jansson ^[1] ; Sumit,Sahni ^[1] ; Darius J R,Lane ^[1] ; Zaklina,Kovacevic ^[1] ; Danuta S,Kalinowski ^[3] ; Des R,Richardson ^[4]

作者单位： Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Blackburn Building (D06), University of Sydney, Sydney, New South Wales 2006, Australia. ^[1] Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Blackburn Building (D06), University of Sydney, Sydney, New South Wales 2006, Australia; Department of Nutrition and Dietetics, Faculty of Medicine and Health Sciences, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia. ^[2] Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Blackburn Building (D06), University of Sydney, Sydney, New South Wales 2006, Australia. Electronic address: danutak@med.usyd.edu.au. ^[3] Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Blackburn Building (D06), University of Sydney, Sydney, New South Wales 2006, Australia. Electronic address: d.richardson@med.usyd.edu.au. ^[4]

关键词 Anti-cancer drug Dp44mT Endoplasmic reticulum Endoplasmic reticulum stress Unfolded protein response