期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：17
页码：6770-6773
DOI：10.1073/pnas.0401604101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Apoptotic volume decrease is a pivotal event triggering a cell to undergo apoptosis and is induced by ionic effluxes resulting mainly from increased K+ and Cl- conductances. Here, we demonstrate that in human epithelia HeLa cells both mitochondrion- and death receptor-mediated apoptosis inducers [staurosporine and Fas ligand or tumor necrosis factor (TNF)-{alpha}] rapidly activate Cl- currents that show properties phenotypical of volume-sensitive outwardly rectifying Cl- channel currents, including outward rectification, voltage-dependent inactivation gating at large positive potentials, inhibition by osmotic shrinkage, sensitivity to classic Cl- channel blockers, and dependence on cytosolic ATP. Staurosporine, but not Fas ligand or TNF-{alpha
