scholarly journals Correction: A ratiometric fluorescent probe for peroxynitrite prepared by de novo synthesis and its application in assessing the mitochondrial oxidative stress status in cells and in vivo

2018 ◽  
Vol 54 (93) ◽  
pp. 13159-13159 ◽  
Author(s):  
Dong-Ye Zhou ◽  
Yongfei Li ◽  
Wen-Li Jiang ◽  
Yang Tian ◽  
Junjie Fei ◽  
...  

Correction for ‘A ratiometric fluorescent probe for peroxynitrite prepared by de novo synthesis and its application in assessing the mitochondrial oxidative stress status in cells and in vivo’ by Dong-Ye Zhou et al., Chem. Commun., 2018, 54, 11590–11593.

2018 ◽  
Vol 54 (82) ◽  
pp. 11590-11593 ◽  
Author(s):  
Dong-Ye Zhou ◽  
Yongfei Li ◽  
Wen-Li Jiang ◽  
Yang Tian ◽  
Junjie Fei ◽  
...  

A ratiometric fluorescent probe is prepared by de novo synthesis for assessing the mitochondrial oxidative stress status in cells and in vivo.


2018 ◽  
Vol 90 (12) ◽  
pp. 7467-7473 ◽  
Author(s):  
Feiyan Liu ◽  
Zhen Wang ◽  
Wenli Wang ◽  
Jian-Guang Luo ◽  
Lingyi Kong

2017 ◽  
Vol 5 (42) ◽  
pp. 8389-8398 ◽  
Author(s):  
Kun Dou ◽  
Guang Chen ◽  
Fabiao Yu ◽  
Zhiwei Sun ◽  
Guoliang Li ◽  
...  

We report herein a mitochondria-targeted two-photon ratiometric fluorescent probe to respectively or successively detect HSO3−/HClO in cells and zebrafish.


2016 ◽  
Vol 113 (43) ◽  
pp. E6669-E6678 ◽  
Author(s):  
Mark A. Gregory ◽  
Angelo D’Alessandro ◽  
Francesca Alvarez-Calderon ◽  
Jihye Kim ◽  
Travis Nemkov ◽  
...  

Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are common in acute myeloid leukemia (AML) and drive leukemic cell growth and survival. Although FLT3 inhibitors have shown considerable promise for the treatment of AML, they ultimately fail to achieve long-term remissions as monotherapy. To identify genetic targets that can sensitize AML cells to killing by FLT3 inhibitors, we performed a genome-wide RNA interference (RNAi)-based screen that identified ATM (ataxia telangiectasia mutated) as being synthetic lethal with FLT3 inhibitor therapy. We found that inactivating ATM or its downstream effector glucose 6-phosphate dehydrogenase (G6PD) sensitizes AML cells to FLT3 inhibitor induced apoptosis. Examination of the cellular metabolome showed that FLT3 inhibition by itself causes profound alterations in central carbon metabolism, resulting in impaired production of the antioxidant factor glutathione, which was further impaired by ATM or G6PD inactivation. Moreover, FLT3 inhibition elicited severe mitochondrial oxidative stress that is causative in apoptosis and is exacerbated by ATM/G6PD inhibition. The use of an agent that intensifies mitochondrial oxidative stress in combination with a FLT3 inhibitor augmented elimination of AML cells in vitro and in vivo, revealing a therapeutic strategy for the improved treatment of FLT3 mutated AML.


Author(s):  
Tonghui Huang ◽  
Shirong Yan ◽  
Yongbo Yu ◽  
Yunsheng Xue ◽  
Yanyan Yu ◽  
...  

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