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Some amphiphilic cations block the mitochondrial apoptosis‐induced channel, MAC
Author(s) -
Martinez-Caballero Sonia,
Dejean Laurent M,
Kinnally Kathleen W
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.05.006
Subject(s) - amphiphile , chemistry , apoptosis , block (permutation group theory) , biophysics , mitochondrial apoptosis induced channel , mitochondrion , microbiology and biotechnology , inner mitochondrial membrane , biochemistry , biology , copolymer , organic chemistry , combinatorics , mathematics , polymer
The mitochondrial apoptosis‐induced channel (MAC) forms in the outer membrane of mitochondria early in apoptosis and this activity is altered by physiological levels of cytochrome c . While cyclosporine A and lidocaine have no effect, dibucaine induces a fast blockade of MAC with an IC 50 of 39 μM. In contrast, the IC 50 for propranolol and trifluoperazine are 52 and 0.9 μM, respectively, and these drugs likely destabilize the open state of MAC. These agents, and others not yet identified, should be valuable tools in the study of apoptosis. Profiling MAC's pharmacology may generate novel therapeutic regimes for disease.