O-Glycosylation of transcription factor BCL11b: truth or myth? Public Deposited

http://ir.library.oregonstate.edu/concern/undergraduate_thesis_or_projects/qn59q5305

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  • BCL11B, a gene regulatory transcription factor, is known to be a regulator of T cell development in the immune system, and has been identified as a tumor suppressor for T cell leukemias. Defining the molecular events that regulate the activity of BCL11B will provide potential drug targets that will aid those with T cell leukemia. In addition, the development of T cells will be better understood, providing more knowledge of the immune system. We know that BCL11B activity changes when developing T cells (known as thymocytes) are stimulated and that this activity change coincides with changes in the levels of phosphorylation and sumoylation of the factor. Additionally, we know that many nuclear proteins are modified by O-glycosylation, and that this modification is often mutually exclusive with phosphorylation. Working in Dr. Filtz’s lab this winter term, I obtained preliminary evidence that BCL11B is O-glycosylated. We investigated BCL11B for O-glycosylation and discovered that BCL11B is not glycosylated, but changing glycosylation levels in the system changes the phosphorylation of BCL11B.
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