Introduction of the beta isozyme of protein kinase C accelerates induced differentiation of murine erythroleukemia cells.

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Abstract
Induction of differentiation in murine erythroleukemia cells (MELCs) involves a protein kinase C (PKC)-mediated step. Vincristine-resistant cells respond more rapidly to hybrid polar/apolar inducers than the parental cells. These vincristine-resistant MELCs contain elevated levels of the .beta. isozyme of PKC (PKC-.beta.). Exogenous homologous murine PKC-.beta., incorporated into permeabilized MELCs, accelerates induced differentiation. Neither rat PKC-.beta., nor mouse PKC-.alpha., nor rat PKC-.alpha., incorporated into permeabilized MELCs, is effective in altering the kinetics of induced differentiation. This provides direct evidence for a rate-limiting role for this PKC isozyme during N,N''-hexamethylenebisacetamide-mediated induced differentiation of a transformed cell.