Mitochondrial Translocation of Protein Kinase C δ in Phorbol Ester-induced Cytochrome c Release and Apoptosis

Apoptosis is induced by the release of cytochromec from mitochondria to the cytoplasm. The present studies demonstrate that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) induces translocation of protein kinase C (PKC) δ from the cytoplasm to mitochondria. The results also show that tr...

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Bibliographic Details
Published in:The Journal of biological chemistry 2000-07, Vol.275 (29), p.21793-21796
Main Authors: Majumder, Pradip K., Pandey, Pramod, Sun, Xiangao, Cheng, Keding, Datta, Rakesh, Saxena, Satya, Kharbanda, Surender, Kufe, Donald
Format: Article
Language:English
Subjects:
Apoptosis - drug effects
Apoptosis - physiology
Carcinogens - pharmacology
Cytochrome c Group - metabolism
Humans
Isoenzymes - metabolism
Mitochondria - metabolism
Protein Kinase C - metabolism
Protein Kinase C-delta
Tetradecanoylphorbol Acetate - pharmacology
U937 Cells
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Summary:Apoptosis is induced by the release of cytochromec from mitochondria to the cytoplasm. The present studies demonstrate that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) induces translocation of protein kinase C (PKC) δ from the cytoplasm to mitochondria. The results also show that translocation of PKCδ results in release of cytochrome c. The functional significance of this event is further supported by the demonstration that PKCδ translocation is required for TPA-induced apoptosis. These findings demonstrate that translocation of PKCδ to mitochondria is responsible, at least in part, for inducing cytochrome crelease and apoptosis.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.C000048200