Involvement of PP6 in Dephosphorylation of Bcl11b, a Tumor Suppressor Transcription Factor


The purpose of this honors thesis research project is to investigate the molecular causes of childhood and infant T-cell acute lymphoblastic leukemias. T-cells are the work horses of the immune system, and like any organ, must develop properly to be fully functional. Improper development of thymocytes into T-cells can lead to development of T-cell leukemias and lymphomas. Regulation of thymocyte development is coordinated by transcription factors, of which Bcl1 1b is essential for proper T-cell development. Bcl1 1b is regulated by phosphorylation and dephosphorylation. Previously, a correlation was found between dephosphorylation of Bcl1 1b and increased expression of Id2 in developing T-cells. Regulation of the tumorigenic Id2 gene is crucial for proper T-cell development. Based on preliminary studies, we hypothesized that PP6 is the phosphatase responsible for dephosphorylating Bcl11b and altering transcriptional activity of the Id2 gene. DNA constructs for PP6 and Bcl11b proteins were transfected into HEK-293T cells, and then cells were lysed and assayed for Bcl11b phosphorylation. Our results indicated that PP6 co-expression increased Bcl11b dephosphorylation in HEK-293T cells. However, reporter gene assays showed that PP6 co-expression has no effect on Bcl11b-dependent repression of the Id2 promoter in transfected HEK-293T cells. The\ud next step is to investigate whether PP6 down-regulation of Bcl1 1b affects Id2 expression in native thymocytes

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This paper was published in ScholarsArchive@OSU.

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