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Functional inactivation of wild-type p53 protein correlates with loss of IL-2 dependence in HTLV-I transformed human T lymphocytes.




 

Leukemia. 1995 Dec;9(12):2082-6. Unique Identifier : AIDSLINE

Human T cell leukemia virus type-I (HTLV-I), the etiologic agent of adult T cell leukemia (ATL) transforms human T cells in vitro and in vivo. Tax, the major transactivator of HTLV-I is critical for the initial events involved in transformation, however, the later steps required for progression from an IL-2 dependent state to one of IL-2 independence remain to be clarified. We investigated the potential role of p53 protein in this process employing several IL-2 dependent and independent HTLV-I transformed cell lines. All cell lines examined were found to be wild-type in the p53 coding region usually associated with inactivating mutations using RT-PCR-SSCP analysis and DNA sequencing. Levels of p53 protein were consistently higher in IL-2 independent lines compared to IL-2 dependent ones. Lack of functional p53 activity was observed only in IL-2 independent cell lines using a transfection assay with a B-galactosidase reporter gene construct responsive to wild-type p53 protein. Increased steady state levels of wild-type p53 protein associated with its functional inactivation appear to be linked to the loss of IL-2 dependent growth in HTLV-I transformed lymphocytes.

Base Sequence *Cell Transformation, Viral Cells, Cultured Human *HTLV-I Interleukin-2/*PHARMACOLOGY Molecular Sequence Data Mutation Protein p53/GENETICS/*METABOLISM Support, Non-U.S. Gov't T-Lymphocytes/METABOLISM/*VIROLOGY Trans-Activation (Genetics) JOURNAL ARTICLE



 




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