scholarly journals Mitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib‐resistantBRAFV600Emutation bearing metastatic melanoma cells

2019 ◽  
Vol 58 (9) ◽  
pp. 1680-1690 ◽  
Author(s):  
Evan L. Carpenter ◽  
Sharmeen Chagani ◽  
Dylan Nelson ◽  
Pamela B. Cassidy ◽  
Madeleine Laws ◽  
...  
2017 ◽  
Vol 40 (6) ◽  
pp. 583-594.e6 ◽  
Author(s):  
Evan A. Bordt ◽  
Pascaline Clerc ◽  
Brian A. Roelofs ◽  
Andrew J. Saladino ◽  
László Tretter ◽  
...  

2019 ◽  
Vol 18 (8) ◽  
pp. e3041
Author(s):  
B. Schöpf ◽  
H. Weissensteiner ◽  
G. Schäfer ◽  
A. Naschberger ◽  
B. Rupp ◽  
...  

2014 ◽  
Vol 15 (5) ◽  
pp. 487-501 ◽  
Author(s):  
Darka Šešlija Jovanović ◽  
Mirko Đorđević ◽  
Uroš Savković ◽  
Jelica Lazarević

2019 ◽  
Vol 27 (12) ◽  
pp. 2444-2448 ◽  
Author(s):  
Nadine Kaiser ◽  
Dale Corkery ◽  
Yaowen Wu ◽  
Luca Laraia ◽  
Herbert Waldmann

2000 ◽  
Vol 55 (7-8) ◽  
pp. 620-630 ◽  
Author(s):  
Gerhard Bringmann ◽  
Doris Feineis ◽  
Ralf God ◽  
Ralph Brückner ◽  
Jens Achim-Protzen ◽  
...  

Abstract Several N-alkanoyl derivatives (4-9 and 13-16) of the potent mitochondrial complex I inhibitor TaClo (1-trichlorom ethyl-1,2,3,4-tetrahydro-β-carboline, 2) have been synthesized in order to elucidate the role of hydrophobic portion in the inhibitory action. Using rat brain homogenates or submitochondrial particles, the inhibitory effects of these compounds towards NADH-ubiquinone reductase (complex I) activity indeed appeared to correlate quite strongly with their lipophilic character. An X-ray structure analysis, exemplarily performed for N-acetyl-TaClo (4), revealed the N-substituent of such chlorinated agents to be dramatically pushed out of the β-carboline ring ‘plane’ due to the high steric demand of the huge trichloromethyl group at C-1.


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