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Differential Correlation Between Translocation and Down‐Regulation of Conventional and New Protein Kinase C Isozymes in C 6 Glioma Cells
Author(s) -
Chen Ching Chow,
Cheng Chin San,
Chang Jacque,
Huang Huei Chen
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64020818.x
Subject(s) - isozyme , chromosomal translocation , glioma , biology , differential (mechanical device) , microbiology and biotechnology , protein kinase a , kinase , chemistry , biophysics , biochemistry , enzyme , genetics , gene , physics , thermodynamics
Correlation between translocation and down‐regulation of conventional protein kinase Cα (cPKCα) and new PKCδ (nPKCδ) induced by 12‐ O ‐tetradecanoylphorbol 13‐acetate (TPA) at different time courses (5 min, 30 min, 1 h, 3 h, 6 h, 10 h, 17 h, and 24 h) was studied in C 6 glioma cells. From the dose‐dependent translocations of these two isoforms by 10‐min treatment with TPA (1, 3, 10, 30, 100, 300, and 1,000 n M ), we found that cPKCα was translocated by 3–1,000 n M and nPKCδ was translocated by 10–1,000 n M TPA. Both isoforms were maximally translocated by 100–1,000 n M TPA, whereas 1 n M did not translocate these two isoforms. When the cells were treated with 1,000 n M TPA for 5 min to 17 h, the translocation of these two isoforms occurred rapidly after 5‐min treatment and could be sustained for 1 h, whereas down‐regulation occurred after 3‐h treatment and almost complete down‐regulation was observed after 17‐h treatment. However, the extent of down‐regulation of nPKCδ was greater than that of cPKCα at 3‐, 6‐, and 10‐h treatment. Further studies by using different doses of TPA (100, 10, 3, and 1 n M ) and extending the time to 24 h showed that cPKCα was more resistant to down‐regulation. This conventional isoform was maintained at a translocation state even after long‐term treatment with 3–100 n M TPA, and complete down‐regulation was only shown after 1,000 n M treatment. On the other hand, nPKCδ was almost completely down‐regulated by long‐term treatment with a translocation dose of 10–1,000 n M TPA despite higher membrane content of this new isoform. Therefore, the differential translocation and down‐regulation of cPKCα and nPKCδ was demonstrated in C 6 glioma cells and this will be useful for exploring cPKCα‐ or nPKCδ‐specific functional roles in cellular functions and different signal transduction pathways in these cells.