@article{14ce1f7aa6aa4dd694a9ec466de8e384,
title = "Marine natural product aurilide activates the opa1-mediated apoptosis by binding to prohibitin",
abstract = "Aurilide is a potent cytotoxic marine natural product that induces apoptosis in cultured human cells at the picomolar to nanomolar range; however, its mechanism of action has been unknown. Results of the present study showed that aurilide selectively binds to prohibitin 1 (PHB1) in the mitochondria, activating the proteolytic processing of optic atrophy 1 (OPA1) and resulting in mitochondria-induced apoptosis. The mechanism of aurilide cytotoxicity suggests that PHB1 is an apoptosis-regulating protein amenable to modulation by small molecules. Aurilide may serve as a small-molecule tool for studies of mitochondria-induced apoptosis.",
author = "Sato, {Shin Ichi} and Asako Murata and Tsubasa Orihara and Takashi Shirakawa and Kiyotake Suenaga and Hideo Kigoshi and Motonari Uesugi",
note = "Funding Information: This work was supported in part by grants from MEXT(JSPS) KAKENHI (grant 21310140 to M.U. and grant 21870016 to S.S.), the Uehara Memorial Foundation (support to M.U.), the Naito Foundation (support to S.S.), and National Institutes of Health (grant CA109277 to M.U.). We thank H. Hoshi, K. Kajiwara, S. Kuribayashi, and the members of the Uesugi research group for helpful discussion and support. We would also like to thank K. Yamada (Professor Emeritus, Nagoya University) for his long-term support and encouragement. NMR spectra were obtained at the Keck NMR facility of the University of Houston. The Kyoto research group participates in the Global COE program “Integrated Material Sciences” (#B-09). A.M. is an Inoue Fellow supported by the Inoue Foundation of Science. ",
year = "2011",
month = jan,
day = "28",
doi = "10.1016/j.chembiol.2010.10.017",
language = "English",
volume = "18",
pages = "131--139",
journal = "Cell Chemical Biology",
issn = "2451-9448",
publisher = "Elsevier Inc.",
number = "1",
}
