Mcl-1 is a pro-survival relative of Bcl-2 and its over-activity is implicated in tumorigenesis as well as resistance to standard-of-care agents used to treat cancer patients. It is a very labile protein with a half-life of less than 30 minutes. Interestingly, stabilisation of Mcl-1 can promote tumour formation.
Thus, we are interested in elucidating mechanisms that promote Mcl-1 turnover especially those that might be subverted in cancer cells. We are actively investigating ways that might promote Mcl-1 degradation as a means to indirectly target Mcl-1 for the treatment of cancers.