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 vineristine-resistant MELCs contain elevated levels of the β isozyme of PKC (PKC-β). Exogenous homologous murine PKC-β, incorporated into permeabilized MELCs, accelerates induced differentiation. Neither rat PKC-β, nor mouse PKC-α, rat PKC-α, 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. |
Keywords: |
controlled study; unclassified drug; nonhuman; animal cell; mouse; animal; mice; cell division; cell line; animal experiment; hemoglobin; vincristine; cell differentiation; drug resistance; tumor cells, cultured; animalia; kinetics; cell culture; brain; murinae; immunoblotting; protein kinase c; rats; cell density; enzyme purification; isoenzymes; protein kinase c alpha; induction; isoenzyme; protein kinase c beta; leukemia, erythroblastic, acute; commitment; hexamethylenebisacetamide; acetamides; priority journal; article; leukemia, experimental; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; erythroleukemia cell; beta isoenzyme
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