Honors College Thesis

 

Factors that Modify and Control Bcl11b, a Tumor Suppressor Protein Public

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  • The experiments explained in this Honors thesis are focused on finding a cellular model for analyzing Bcl11b, a transcription factor dysregulated in 20% of cases of T-cell Acute Lymphoblastic Leukemia (T-ALL). Acute Lymphoblastic Leukemia is the most common childhood cancer. Because T-ALL is a result of incorrect thymocyte development, research into how T-cells mature is essential. A key factor in T-cell maturation is the transcription factor Bcl11b. Two key Bcl11b post-translational modifications include phosphorylation and sumoylation, of which Bcl11b has 23 and 2 sites, respectively. The first experiments attempted to identify an ideal model for studying Bcl11b; however both cellular models tested had negative characteristics. Mouse thymocytes could not be transfected using the Invitrogen Neon® Electroporation System. P2C2 cells post-translationally modified Bcl11b differently than thymocytes. The next experiment was to identify which of Bcl11b’s phosphorylation sites contribute more towards the composite phosphorylation level and was more important in cell signaling. This was done with Bcl11b mutants that had key phosphorylation sites eliminated. While initial data suggested that mutating phosphorylation sites affected overall phosphorylation levels, subsequent experiments resulted in conflicting data suggesting that the number of phosphorylation sites eliminated had little effect on the expressed composite phosphorylation level of Bcl11b.
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