PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16534736-0 2006 Inhibitory effects of ginsenoside-Rb1 on activation of the 12-O-tetradecanoylphorbol 13-acetate-induced cyclooxygenase-2 promoter. Tetradecanoylphorbol Acetate 59-95 RB transcriptional corepressor 1 Homo sapiens 34-37 16534736-1 2006 We studied the inhibitory effects of ginsenoside-Rb1 (1) on 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced transcriptional activation of the cyclooxygenase-2 (COX-2) promoter. Tetradecanoylphorbol Acetate 60-96 RB transcriptional corepressor 1 Homo sapiens 49-52 16534736-1 2006 We studied the inhibitory effects of ginsenoside-Rb1 (1) on 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced transcriptional activation of the cyclooxygenase-2 (COX-2) promoter. Tetradecanoylphorbol Acetate 98-101 RB transcriptional corepressor 1 Homo sapiens 49-52 16534736-3 2006 Ginsenoside-Rb1 at 100 microM inhibited TPA-induced transcriptional activation of the COX-2 promoter. Tetradecanoylphorbol Acetate 40-43 RB transcriptional corepressor 1 Homo sapiens 12-15 11289135-7 2001 FP accelerated PMA-mediated dephosphorylation of the retinoblastoma protein (pRb), an event followed by pRb cleavage culminating in the complete loss of underphosphorylated pRb (approximately Mr 110,000) by 24 h. Finally, gel shift analysis revealed that coadministration of FP with PMA for 8 h led to diminished E2F/pRb binding compared to the effects of PMA alone. Tetradecanoylphorbol Acetate 15-18 RB transcriptional corepressor 1 Homo sapiens 77-80 16534736-7 2006 In conclusion, ginsenoside-Rb1 inhibits TPA-induced COX-2 promoter activity through the nuclear factor interleukin-6 binding site and not through the nuclear factor-kappaB or cAMP-responsive elements. Tetradecanoylphorbol Acetate 40-43 RB transcriptional corepressor 1 Homo sapiens 27-30 15649406-6 2005 Downstream of PKC, PMA treatment inhibited extracellular signal-regulated kinase mitogen-activated protein kinase phosphorylation, up-regulated c-jun NH(2)-terminal kinase phosphorylation, and inhibited retinoblastoma (Rb) phosphorylation. Tetradecanoylphorbol Acetate 19-22 RB transcriptional corepressor 1 Homo sapiens 203-217 15649406-6 2005 Downstream of PKC, PMA treatment inhibited extracellular signal-regulated kinase mitogen-activated protein kinase phosphorylation, up-regulated c-jun NH(2)-terminal kinase phosphorylation, and inhibited retinoblastoma (Rb) phosphorylation. Tetradecanoylphorbol Acetate 19-22 RB transcriptional corepressor 1 Homo sapiens 219-221 11591175-4 2001 pRb is dephosphorylated in the presence of p21-CDK2/4 complexes, and the Rb-E2F1 complex increases after TPA treatment, whereas the Rb-HDAC1 complex decreases slightly. Tetradecanoylphorbol Acetate 105-108 RB transcriptional corepressor 1 Homo sapiens 0-3 11041200-2 2000 TPA-induced PKC activation resulted in dephosphorylation of pRb and subsequently induced ML-1 differentiation based on morphological changes and CD14 expression. Tetradecanoylphorbol Acetate 0-3 RB transcriptional corepressor 1 Homo sapiens 60-63 11041200-4 2000 Preinhibition of PP-1 and PP-2a activities with 1-100 nM okadaic acid dose-dependently blunted the decrease in the phosphorylation status of pRb obtained with TPA and overrode cell cycle arrest. Tetradecanoylphorbol Acetate 159-162 RB transcriptional corepressor 1 Homo sapiens 141-144 1338571-3 1992 Treatment of the cells with the phorbol ester, tetradecanoyl phorbol acetate (TPA), resulted in both a loss of the heterogeneity of the pRB species and a significant decrease in the level of pRB phosphorylation. Tetradecanoylphorbol Acetate 47-76 RB transcriptional corepressor 1 Homo sapiens 136-139 9615391-8 1998 In addition, bryostatin 1 was less effective than PMA in dephosphorylating pRb, modifying E2F complexes, and downregulating c-Myc. Tetradecanoylphorbol Acetate 50-53 RB transcriptional corepressor 1 Homo sapiens 75-78 9615391-9 1998 Co-administration of bryostatin 1 with PMA antagonized the latter"s differentiation-inducing capacity and anti-proliferative effects, actions that were accompanied by a reduction in PMA-mediated p21CIP1/WAF1 induction, CDK2 inhibition, pRb dephosphorylation, and c-Myc downregulation. Tetradecanoylphorbol Acetate 39-42 RB transcriptional corepressor 1 Homo sapiens 236-239 1338571-3 1992 Treatment of the cells with the phorbol ester, tetradecanoyl phorbol acetate (TPA), resulted in both a loss of the heterogeneity of the pRB species and a significant decrease in the level of pRB phosphorylation. Tetradecanoylphorbol Acetate 47-76 RB transcriptional corepressor 1 Homo sapiens 191-194 1338571-3 1992 Treatment of the cells with the phorbol ester, tetradecanoyl phorbol acetate (TPA), resulted in both a loss of the heterogeneity of the pRB species and a significant decrease in the level of pRB phosphorylation. Tetradecanoylphorbol Acetate 78-81 RB transcriptional corepressor 1 Homo sapiens 136-139 1338571-3 1992 Treatment of the cells with the phorbol ester, tetradecanoyl phorbol acetate (TPA), resulted in both a loss of the heterogeneity of the pRB species and a significant decrease in the level of pRB phosphorylation. Tetradecanoylphorbol Acetate 78-81 RB transcriptional corepressor 1 Homo sapiens 191-194 1338571-6 1992 These results are consistent with a model in which TPA and dibutyryl cAMP dependent pathways can activate pRB by altering its phosphorylation. Tetradecanoylphorbol Acetate 51-54 RB transcriptional corepressor 1 Homo sapiens 106-109