PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16368122-5 2006 Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice. Tetradecanoylphorbol Acetate 8-11 Kirsten rat sarcoma viral oncogene homolog Mus musculus 77-82 3409475-6 1988 In contrast, another single-step, high dose MCA transformant (MCACl#16/39) known to contain an activated c-Ki-ras gene shows TPA-independent focus formation in mixed culture with C3H/10T1/2 cells, anchorage independence and tumorigenicity. Tetradecanoylphorbol Acetate 125-128 Kirsten rat sarcoma viral oncogene homolog Mus musculus 105-113 12151388-12 2002 Furthermore, K-Ras, the isoform previously shown to bind to calmodulin, is the only one activated by TPA when calmodulin is inhibited. Tetradecanoylphorbol Acetate 101-104 Kirsten rat sarcoma viral oncogene homolog Mus musculus 13-18 12151388-14 2002 In vitro experiments showed that the phosphorylation of K-Ras by PKC was inhibited by calmodulin, suggesting that calmodulin-dependent modulation of K-Ras phosphorylation by PKC could be the mechanism underlying K-Ras activation in fibroblasts treated with TPA plus W13. Tetradecanoylphorbol Acetate 257-260 Kirsten rat sarcoma viral oncogene homolog Mus musculus 56-61 12151388-14 2002 In vitro experiments showed that the phosphorylation of K-Ras by PKC was inhibited by calmodulin, suggesting that calmodulin-dependent modulation of K-Ras phosphorylation by PKC could be the mechanism underlying K-Ras activation in fibroblasts treated with TPA plus W13. Tetradecanoylphorbol Acetate 257-260 Kirsten rat sarcoma viral oncogene homolog Mus musculus 149-154 12151388-14 2002 In vitro experiments showed that the phosphorylation of K-Ras by PKC was inhibited by calmodulin, suggesting that calmodulin-dependent modulation of K-Ras phosphorylation by PKC could be the mechanism underlying K-Ras activation in fibroblasts treated with TPA plus W13. Tetradecanoylphorbol Acetate 257-260 Kirsten rat sarcoma viral oncogene homolog Mus musculus 149-154 9819387-8 1998 The C1 domain could also confer phorbol myristate acetate-regulated transforming activity on a prenylation-defective mutant of K-Ras. Tetradecanoylphorbol Acetate 32-57 Kirsten rat sarcoma viral oncogene homolog Mus musculus 127-132