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- W1994906239 abstract "This study tested the hypothesis that mitochondrial precursor targeting peptides can elicit the release of cytochrome c from both liver and brain mitochondria by a mechanism distinct from that mediated by the classical, Ca2+-activated permeability transition pore. Human cytochrome oxidase subunit IV signal peptide (hCOXIV1-22) at concentrations from 15 to 100 microM induced swelling, a decrease in membrane potential, and cytochrome c release in both types of mitochondria. Although cyclosporin A and bongkrekic acid were without effect, dibucaine, propanolol, dextran, and the uncoupler FCCP were each able to inhibit signal peptide-induced swelling and cytochrome c release. Adenylate kinase was coreleased with cytochrome c, arguing against a signal peptide-induced cytochrome c-specific pathway of efflux across the outer membrane. Taken together, the data indicate that a human mitochondrial signal peptide can evoke the release of cytochrome c from both liver and brain mitochondria by a unique permeability transition that differs in several characteristics from the classical mitochondrial permeability transition." @default.
- W1994906239 created "2016-06-24" @default.
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- W1994906239 date "2001-02-01" @default.
- W1994906239 modified "2023-09-26" @default.
- W1994906239 title "Mitochondrial Precursor Signal Peptide Induces a Unique Permeability Transition and Release of Cytochrome c from Liver and Brain Mitochondria" @default.
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- W1994906239 doi "https://doi.org/10.1006/abbi.2000.2201" @default.
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