The Catalytic Domain of Protein Kinase C-δ in Reciprocal δ and ϵ Chimeras Mediates Phorbol Ester-induced Macrophage Differentiation of Mouse Promyelocytes

摘要: The overexpression of protein kinase C-delta (PKC-delta), but not PKC-epsilon, enables the mouse myeloid cell line 32D to differentiate into macrophages when treated with phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). To determine domain PKC-delta that is responsible for this isotype-specific function, cDNAs encode reciprocal chimeras and -epsilon (PKC-delta epsilon PKC-epsilon delta) were constructed by exchanging regulatory domains using polymerase chain reaction technology. Both stably expressed in cells pLTR expression vector displayed activity upon TPA treatment. treatment L delta, overexpressed delta chimera, induced a dramatically increased volume, surface adherence, Mac-1 Mac-3, lysozyme production, phagocytosis. These are characteristics macrophage phenotype found TPA-treated PKC-delta. In contrast, little effect was seen epsilon, or without A PKC inhibitor directed toward catalytic PKC, GF109203X, selective PKC-delta, Rottlerin, blocked TPA-induced differentiation delta-overexpressing cells. results demonstrate contains primary determinants its ester-induced differentiation.