cDNA Cloning and Mapping of Mouse Pleckstrin (Plek), a Gene Upregulated in Transformation-Resistant Cells
Autor: | Bernard Gerrard, Glenn Hegamyer, Michael Dean, Joan L. Cmarik, Nancy H. Colburn |
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Rok vydání: | 2000 |
Předmět: |
DNA
Complementary Molecular Sequence Data Biology medicine.disease_cause Mice Sequence Homology Nucleic Acid Complementary DNA Gene expression Genetics medicine Animals Humans Neoplastic transformation Amino Acid Sequence Cloning Molecular Differential display Base Sequence Blood Proteins DNA Phosphoproteins Molecular biology Up-Regulation Pleckstrin homology domain Cell Transformation Neoplastic Cell culture Tumor promotion Carcinogenesis |
Zdroj: | Genomics. 66:204-212 |
ISSN: | 0888-7543 |
DOI: | 10.1006/geno.2000.6210 |
Popis: | 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 approximately 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. |
Databáze: | OpenAIRE |
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