Abstract: |
Induction of erythroid differentiation of murine erythroleukemia cells (MELC) by exposure to hexamethylene bisacetamide (HMBA) involves the modulation of protein kinase C (PKC) activity. Using immuno- and Northern blot techniques, we have demonstrated that MELC express a pattern of PKC isoforms which includes PKCα, PKCδ, PKCε, PKCζ, and PKCη. We show that MELC resistant to induction by HMBA express significantly less of the nPKC isoform, PKCδ slightly less PKC. Recovery of HMBA sensitivity is associated with reexpression of PKCδ protein. Upon exposure to HMBA, there is a fall in cytosolic PKCδ and PKCε accompanied by a transient increase in membrane-associated forms of these PKC isoforms. HMBA-resistant MELC fail to display this isoform-specific translocation of PKC. Induction of differentiation is accompanied, over the next 24 h of exposure to HMBA, by a progressive fall in cellular PKC activity, associated with a progressive fall in the cellular content of PKCδ, PKCε, and PKCζ. These studies suggest that PKCδ, and possibly PKCε and PKCζ as well, play a role in the pathway of HMBA-mediated terminal cell differentiation of MELC. © 1993, American Association for Cancer Research. All rights reserved. |
Keywords: |
nonhuman; animal cell; animal; mice; cell line; cell differentiation; enzyme activity; immunoblotting; protein kinase c; blotting, northern; enzyme purification; enzyme assay; isoenzymes; cell lysate; isoenzyme; leukemia, erythroblastic, acute; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; erythroleukemia cell
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