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This study investigates the impact of inhibiting the Jun kinase pathway on DNA repair, p53-mediated apoptosis, and gene amplification. Using two experimental systems, mouse embryonic fibroblasts (MEFs) and a lung tumor cell line with K-Ras mutation, the research uncovers the role of Jun kinase in these processes. The findings suggest that blocking the Jun kinase pathway can lead to enhanced p53-mediated apoptosis and gene amplification, shedding light on potential therapeutic approaches for cancer treatment.
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Cell Growth & Differentiation Vol. 10, 545-554, 1999 Inhibition of the Jun Kinase Pathway Blocks DNA Repair, Enhances p53-mediated Apoptosis and Promotes Gene Amplification Ruth A. Gjerset, Svetlana Lebedeva, Ali Haghighi, Sally T. Turla and Dan Mercola
Two independent experiment system (1) MEFs: Mouse Embryonic Fibroblast p53 + or - DNA damage (Doxorubicin; a drug used in cancer chemotherapy) (2) A lung tumor cell line derived from mice expressing an oncogenic K-Ras mutation (K-RasG12D) p53 + or -
cre-lox recombination system Cre-Lox recombination involves the targeting of a specific sequence of DNA and splicing it with the help of an enzyme called Cre recombinase.