ISHIKAWA Naoshi Tokyo Metropolitan Institute of Gerontology, Mol. Pathol. Sen. Res. Scient., 分子病理部門, 研究員 (30184485)
TAGUSHI Takahiko Tokyo Metropolitan Institute of Gerontology, Mol. Biol., Sen. Res. Scient., 分子生物学部門, 研究員 (80073005)
FUKUDA Mitsugu Tokyo Metropolitan Institute of Gerontology, Mol. Biol., Assis. Assoc., 分子生物学部門, 助手 (30100126)
AHIMADA Nobuko Tokyo Metropolitan Institute of Gerontology, Mol. Biol., Assis. Assoc., 分子生物学部門, 助手 (60158962)
Since NDP kinase is considered to be a housekeeping enzyme, its possible involvement in cell growth and differentiation has been suggested. In fact, interactions of NDP kinase with DNA polymerase and ribonucleotide reductase, and growth associated increase in the enzyme activity in fission yeast Schizosaccharomyces pombe, slime mold Dictyostelium discoideum, mouse and human cells have been documented. In the present study, when we investigated the consequence of overexpression or disruption of a Saccharomyces cerevisiae YNK gene that encodes NDP kinase, phenotypic behaviors such as growth rate and spore formation were unaffected. Therefore, although several lines of evidence suggest that NDP kinases seem to play important role in cell growth and differentiation, their precise role remains unknown.
During the course of studies on the role of NDP kinase in cell prolifiration using cultured cell lines of rat origin, we realized that NDP kinase activities in the extracts from resting cultured cell lines seemed generally higher than those from normal rat tissues. Therefore, we asked whether NDP kinase activity is related to the ability of infinite cell growth (immortalization), and examined NDP kinase activity in parallel with translation and transcription products in the extracts from four human normal diploid fibroblasts and their corresponding immortalized cells. The enzyme activity was consistently increased in the immortalized cell lines. This increase was associated with increased translation and transcription products. Further, both isoforms were found to be increased.