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cDNA cloning and mapping of mouse pleckstrin (Plek), a gene upregulated in transformation-resistant cells

  1. Author:
    Cmarik, J. L.
    Hegamyer, G.
    Gerrard, B.
    Dean, M.
    Colburn, N. H.
  2. Author Address

    Colburn NH NCI, Gene Regulat Sect, BRL Bldg 560,Room 21-89 Frederick, MD 21701 USA NCI, Gene Regulat Sect, BRL Frederick, MD 21701 USA NCI, Intramural Res Support Program SAIC Frederick Frederick, MD 21701 USA NCI, Lab Genom Divers, Frederick Canc Res & Dev Ctr Frederick, MD 21701 USA
    1. Year: 2000
  1. Journal: Genomics
    1. 66
    2. 2
    3. Pages: 204-212
  2. Type of Article: Article
  1. Abstract:

    Changes that occur during tumor promotion, the rate-limiting phase of multistep carcinogenesis, may offer the best targets for prevention of cancer or reversal of early disease. The murine epidermal JB6 promotion-sensitive (P+) and -resistant (P-) cell lines provide a cell culture model for tumor promoter-induced neoplastic transformation ideally suited to the identification of molecular events that mediate or inhibit transformation. A differential display comparison of P+ and P- cell mRNAs yielded seven differentially expressed sequences. One of the sequences preferentially expressed in P- cells identified an similar to 3.6-kb message that was induced to higher levels in P- cells following exposure to the tumor promoter 12-O-tetradecanoylphorbol acetate than in P+ cells. The message was detected in mRNA from heart, lung, and spleen. cDNA cloning of the P- preferential sequence revealed a high degree of identity to human pleckstrin (PLEK), the major PKC substrate in platelets (Tyers et al., 1988, Nature 333: 470). We report the complete mouse cDNA sequence of pleckstrin and the localization of the gene to chromosome 11, its expression in a nonhematopoetic cell line, and its potential role in blocking neoplastic transformation. [References: 54]

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