Kim, Sung-WooKim, Shin Hwan2017-12-182017-12-182012Kim, S. H. (2012). Tid1 modulation of p53 ubiquitination in breast cancer cells (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/4942http://hdl.handle.net/1880/105943Bibliography: p. 89-103A page is in colour.In this study, we showed that Tumorous Imaginal Disc 1 (Tidl) has the ability to indirectly modulate p53 ubiquitination in breast cancer cells. The over-expression of Tidl expression in MCF-7 cells led to suppression of p53 ubiquitination whereas its suppression led to enhanced ubiquitination. Tid 1 mediated suppression of p53 ubiquitination can enhance p53 half-life but not endogenous p53 level or p53 downstream targets. Over-expression of Tidl alone was unable to decrease the cell viability of MCF-7 cells but its combination with the proteasome inhibitor ALLN, there was a decrease in cell viability. A reduction in ATP level by Tidl over-expression is suggested to be one of the possible mechanisms that may suppress p53 ubiqutination. In summary, we propose that Tid 1 depletes cellular ATP levels, which in tum, inhibits ubiquitination­proteasome machinery, resulting in enhanced stability of p53.xiii, 103 leaves : ill. ; 30 cm.engUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.Tid1 modulation of p53 ubiquitination in breast cancer cellsmaster thesis10.11575/PRISM/4942