The putative oncogene pim-l is frequently activated by proviral insertion of murine leukemia viruses that induce T cell lymphomas. Full-length genomic and cDNA clones of the human homolog PIM-l have been isolated and sequenced. The deduced amino acid sequence reveals homology between PIM-l and protein kinases. PIM-l is expressed in normal B and T lymphocytes and its levels are significantly elevated in several B lymphoid and myeloid cell lines. This gene maps to human chromosome 6p21, a region involved in translocations in some myeloid leukemias (AML and CML). This proposal describes experiments to study: I. the possible involvement of PIM-l in cells carrying the t(6;9) (p21;q33) translocation II. the biochemical characteristics and kinase activity of PIM-l protein by using antibodies to bacterially expressed PIM-l protein and synthetic peptides III. the transforming potential of the PIM-l gene by introducing it into a retroviral vector IV. regulation of tissue-specific PIM-l expression by assaying the ability of 5' and 3' noncoding regulatory regions (of PIM-l gene) to activate the chloramphenicol acetyl transferase gene in transient expression systems V. role of PIM-l in normal growth and differentiation
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