Related Experiment Video
Updated: Aug 10, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
Activation of protein kinase C by crocidolite asbestos in hamster tracheal epithelial cells
M Perderiset1, J P Marsh, B T Mossman
1Department of Pathology, University of Vermont College of Medicine, Burlington 05405.
Abstract:
To determine the mechanisms of cell signalling by asbestos in epithelial cells of the respiratory tract, the activity of protein kinase C (PKC) was examined in hamster tracheal epithelial (HTE) cells exposed to mitogenic concentrations of crocidolite asbestos. In the histone phosphorylation assay, asbestos significantly increased activity of PKC associated with the membrane fraction of HTE cells. However, in contrast to 12-O-tetradecanoylphorbol-13-acetate, which caused redistribution of almost all PKC activity from the cytosolic to the membrane fraction, the majority of the PKC activity was associated with the cytosolic fraction at all time periods examined. Asbestos did not inhibit binding of [3H]phorbol-12,13-dibutyrate to intact HTE cells, whereas binding was inhibited by the phorbol compounds phorbol dibutyrate and phorbol dibenzoate. Thus, crocidolite-induced activation of PKC does not appear to be mediated through the same mechanism as classical phorbol ester tumor promoters, compounds which activate PKC by structurally resembling diacylglycerol.
Related Concept Videos
Intracellular Signaling Cascades
MAPK Signaling Cascades
PI3K/mTOR/AKT Signaling Pathway
GPCRs Regulate Adenylyl Cylase Activity
Two...
cAMP-dependent Protein Kinase Pathways

