Cytotoxicity at concentrations greater than 1μM is noted with both cell lines, and implicates potential cardiac toxicity as an offCardiomyocyte survive. Bortezomib has been shown to have anti-tumor activity in B cell-type malignancies. K562 Bortezomib shows potent specificity to K562 and dose dependent effects on cell health, with a decrease in viability and corresponding increase in cytotoxicity. The increase in caspase-3 signal indicates the mechanism of toxicity is due to apoptosis induction. A decrease in cytotoxicity signal at higher concentrations of bortezomib in the K562 model may be a result of activation kinetics and time-dependent biomaker decay. The cardiomyocytes do not show apparent off target effects on cell health. These results were selected from a poster presented at the European, Middle Eastern and African Society for Biopreservation and Biobanking (ESBB) 2011 Conference. ▶ View the Poster The proteasome inhibitor Bortezomib shows cytotoxic target specificity toward K562 but not cardiomyocytes target effect of Imatinib treatment. An increase in caspase-3/7 signal with K562 cells only indicates the mechanism of toxicity to be specific to apoptosis, with general cytotoxicity indicated in cardiomyocytes. Bortezomib inhibits the 26S proteasome, part of a complex of proteins thought to be required by cancerous cells to multiply and ApoTox-Glo™ Assay Ordering Information 15

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Promega Australia - Monthly online Magazine - January 2012 edition Lees publicatie 10Home