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In the body, cells that are not required are destroyed by a highly regulated cell suicide mechanism known as apoptosis. Apoptosis is regulated via many protein kinases, including protein kinase C (PKC) isoforms. We, therefore, hypothesize that activation of a novel (δ, ε, µ, θ, and ɳ) PKC family members causes apoptosis in megakaryocytic CMK11-5 cells. We will study apoptosis in CMK11-5 cells by Western blotting, flow cytometry, and the DNA ladder method. Preliminary results show there is no change in apoptosis when cells are treated with Gӧ6976 (a PKCα/PKCβ inhibitor) and suggest that PKC isoforms other than PKCα and PKCβ are responsible for apoptosis.
