I have studied the calpain system in acute myeloid leukemia using the 32D and 32Dkit cell lines. Specifically, I characterized the calpain system in the cell lines, and performed calpastatin overexpression and knockdown studies. I found that calpain activity is elevated in the 32D and 32Dkit cells, and calpain inhibition causes apoptosis. Both μ- and m-calpain contribute to the calpain activity in these cell lines. The 32Dkit cells have higher calpain activity than the 32D cells, which I have shown is partially attributed to basal ckit activation. Calpastatin was present in both cell lines, but exists mainly in a degraded form. Calpastatin overexpression lowered calpain activity and provided a growth disadvantage to the 32Dkit cells, but had no effect on 32D cells. Calpastatin knockdown caused a significant increase in calpain activity in the 32D cells, which changed the cell cycle distribution but had no other major effects.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/30589 |
| Date | 07 December 2011 |
| Creators | Farr, Christina |
| Contributors | Berger, Stuart |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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