@article{oai:nagoya.repo.nii.ac.jp:00014832,
 author = {GAO, SIQIANG and MURAKAMI, MASASHI and ITO, HIROMI and FURUHATA, AYAKO and YOSHIDA, KAYO and TAGAWA, YOKO and HAGIWARA, KAZUMI and TAKAGI, AKIRA and KOJIMA, TETSUHITO and SUZUKI, MOTOSHI and BANNO, YOSHIKO and NOZAWA, YOSHINORI and MURATE, TAKASHI},
 issue = {3-4},
 journal = {Nagoya Journal of Medical Science},
 month = {Sep},
 note = {The underlying mechanisms of oncogene-induced phospholipase D (PLD) activation have not been fully elucidated. The effect of the mutated-ras on PLD mRNA was examined using colon cancer cell lines as well as mock- and mutated ras-transfected NIH3T3 cells. Ras-mutation and activation were correlated, and cells with enhanced ras-activation showed increased PLD1 mRNA and protein. Analysis of the 5’ PLD1 promoter using a representative cell line, DLD-1 and also mutated ras-NIH3T3, showed one Sp1-site as the important ras-responsible motif. Sp1 inhibition with mithramycin A and Sp1 siRNA inhibited PLD1 protein expression and its promoter activity. Sp1 but not Sp3 protein level and increased Sp1-motif binding activity were correlated with ras ativation. Furthermore, overexpression of Sp1 in drosophila SL2 cells lacking Sp family proteins increased PLD1 promoter activity. EMSA and chromatin immunoprecipitation assay confirmed the importance of Sp1 protein binding to the Sp1-motif in ras-induced PLD1 mRNA expression.},
 pages = {127--136},
 title = {Mutated RAS Induced PLD1 Gene Expression through Increased Sp1 Trascription Factor},
 volume = {71},
 year = {2009}
}