Inhibition of Sec61-dependent translocation by mycolactone uncouples the integrated stress response from ER stress, driving cytotoxicity via translational activation of ATF4
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Cell Biology,Cellular and Molecular Neuroscience,Immunology
Link
http://www.nature.com/articles/s41419-018-0427-y.pdf
Reference59 articles.
1. George, K. M. et al. Mycolactone: a polyketide toxin from Mycobacterium ulcerans required for virulence. Science 283, 854–857 (1999).
2. Walsh, D. S., Portaels, F. & Meyers, W. M. Buruli ulcer: advances in understanding Mycobacterium ulcerans infection. Dermatol. Clin. 29, 1–8 (2011).
3. Sarfo, F. S., Phillips, R., Wansbrough-Jones, M. & Simmonds, R. E. Recent advances: role of mycolactone in the pathogenesis and monitoring of Mycobacterium ulcerans infection/Buruli ulcer disease. Cell. Microbiol. 18, 17–29 (2016).
4. Hall, B. S. et al. The pathogenic mechanism of the Mycobacterium ulcerans virulence factor, mycolactone, depends on blockade of protein translocation into the ER. PLoS Pathog. 10, e1004061 (2014).
5. McKenna, M., Simmonds, R. E. & High, S. Mechanistic insights into the inhibition of Sec61-dependent co- and post-translational translocation by mycolactone. J. Cell Sci. 129, 1404–1405 (2016).
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