Actinomycin D-induced apoptosis involves the potassium channel Kv1.3

Several cytostatic agents are known to induce apoptosis in T-leukemic cells. Although a variety of studies show the central role of apoptosis in cytostatic drug-induced cell death, many molecular details require definition. Here, we demonstrate that cells genetically deficient for the potassium chan...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2002-07, Vol.295 (2), p.526-531
Main Authors: Bock, Jürgen, Szabó, Ildikò, Jekle, Andreas, Gulbins, Erich
Format: Article
Language:English
Subjects:
Actinomycin D
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Cell Line
Cytotoxic agents
Dactinomycin - pharmacology
Humans
Kv1.3
Kv1.3 Potassium Channel
Potassium Channels - physiology
Potassium Channels, Voltage-Gated
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Summary:Several cytostatic agents are known to induce apoptosis in T-leukemic cells. Although a variety of studies show the central role of apoptosis in cytostatic drug-induced cell death, many molecular details require definition. Here, we demonstrate that cells genetically deficient for the potassium channel Kv1.3 are resistant to apoptosis initiated by the cytostatic drug actinomycin D. Retransfection of Kv1.3 restores sensitivity of the cells to actinomycin D. Cells lacking Kv1.3 fail to respond to actinomycin D with DNA fragmentation, release of cytochrome c, and loss of mitochondrial membrane potential ( ΔΨ m), while cells functionally expressing Kv1.3 rapidly undergo those changes indicative for apoptosis. The data indicate a central role of the ion channel Kv1.3 in actinomycin D-triggered apoptosis.
ISSN:0006-291X
1090-2104
DOI:10.1016/S0006-291X(02)00695-2