Conformation of the Bax C‐terminus regulates subcellular location and cell death
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TLDR
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.Abstract:
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.read more
Citations
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References
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TL;DR: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens.
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Bcl-2 functions in an antioxidant pathway to prevent apoptosis
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TL;DR: Because of the limited number of references allowed, the authors were unable to cite many important papers; they apologize to their authors.