Subcellular localization of the FLT3-ITD oncogene plays a significant role in the production of NOX- and p22^phox-derived reactive oxygen species in acute myeloid leukemia

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• 作者：Jennifer N. Moloney ; Joanna Stanicka ; Thomas G. Cotter ; ^{t.cotter@ucc.ie}
• 关键词：FLT3 ; FMS-like tyrosine kinase 3 receptor ; FLT3-ITD ; FLT3-internal tandem duplication ; FLT3-WT ; FLT3- wild type ; NOX ; NADPH oxidase ; p22phox ; p22 phagocyte oxidase ; ROS ; reactive oxygen species ; AML ; acute myeloid leukemia ; ER ; endoplasmic reticulum ; H2O2 ; hydrogen peroxide ; PO1 ; peroxy orange 1 ; RTK ; receptor tyrosine kinase ; COX ; cyclooxygenase ; DUOX ; dual oxidase ; DMSO ; dimethylsulfoxide
• 刊名：Leukemia Research
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：52
• 期：Complete
• 页码：34-42
• 全文大小：2248 K
• 卷排序：52

文摘

Tunicamycin and Brefeldin A, induce ER retention of FLT3-ITD. ER retention of FLT3-ITD results in post-translational modification of p22phox and NOX4. NOX-generated ROS contribute to total pro-survival ROS in AML. AKT pathway is vital for FLT3-ITD at the plasma membrane oncogenic effects.