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| The EMBO Journal
(1999) 18, 2330–2341, doi:10.1093/emboj/18.9.2330 |
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| Conformation of the Bax C-terminus regulates subcellular location and cell death |
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| Amotz Nechushtan1, Carolyn L. Smith2, Yi-Te Hsu1 and Richard J. Youle1 |
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1 Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA 2 Light Microscopy Facility, Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA To whom correspondence should be addressed Richard J. Youle, youle@helix.nih.gov Received 7 December 1998; Revised 19 February 1999; Accepted 8 March 1999. |
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| Abstract |
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| Bax, a pro-apoptotic member of the Bcl-2 family, translocates from the cytosol to the mitochondria during programmed cell death. We report here that both gain-of-function and loss-of-function mutations can be achieved by altering a single amino acid in the Bax hydrophobic C-terminus. The properly mutated C-terminus of Bax can target a non-relevant protein to the mitochondria, showing that specific conformations of this domain alone allow mitochondrial docking. These data along with N-terminus epitope exposure experiments suggest that the C- and the N-termini interact and that upon triggering of apoptosis, Bax changes conformation, exposing these two domains to insert into the mitochondria and regulate the cell death machinery. |
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| Keywords: apoptosis, Bcl-2, GFP, mitochondria, point mutations |
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