PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 6420041-4 1984 Since alpha-difluoromethylornithine (DFMO) and methylglyoxal-bis-guanylhydrazone (MGBG) are irreversible and competitive inhibitors of ODC and SAMDC, respectively, they were tested as single agents and in combination on a transplantable rapidly growing and hormone-resistant G subline of the Dunning R-3327 rat prostatic adenocarcinoma. Eflornithine 6-35 adenosylmethionine decarboxylase 1 Rattus norvegicus 143-148 1415709-12 1992 Treatment with DL-alpha-difluoromethylornithine (DFMO), a specific ODC inhibitor, prevented the increases in both cellular putrescine levels and SAMDC activity in asparagine- and serum-treated cells. Eflornithine 15-47 adenosylmethionine decarboxylase 1 Rattus norvegicus 145-150 1415709-12 1992 Treatment with DL-alpha-difluoromethylornithine (DFMO), a specific ODC inhibitor, prevented the increases in both cellular putrescine levels and SAMDC activity in asparagine- and serum-treated cells. Eflornithine 49-53 adenosylmethionine decarboxylase 1 Rattus norvegicus 145-150 1415709-13 1992 In the presence of DFMO, exogenous putrescine returned SAMDC activity toward control levels but had no effect on ODC. Eflornithine 19-23 adenosylmethionine decarboxylase 1 Rattus norvegicus 55-60 7899459-9 1995 In contrast, the azaserine-induced significant increase in hepatic putrescine was lower and transient, was accompanied by an increase in ODC and SAM-DC, and was completely inhibited by simultaneous DFMO treatment but not by MDL 72527. Eflornithine 198-202 adenosylmethionine decarboxylase 1 Rattus norvegicus 145-151 2114097-1 1990 S-Adenosylmethionine decarboxylase (AdoMetDC) activity was elevated 18.8-fold in Swiss 3T3 fibroblasts which were depleted of cellular polyamines by using the inhibitor difluoromethylornithine (DFMO). Eflornithine 169-192 adenosylmethionine decarboxylase 1 Rattus norvegicus 0-34 2114097-1 1990 S-Adenosylmethionine decarboxylase (AdoMetDC) activity was elevated 18.8-fold in Swiss 3T3 fibroblasts which were depleted of cellular polyamines by using the inhibitor difluoromethylornithine (DFMO). Eflornithine 169-192 adenosylmethionine decarboxylase 1 Rattus norvegicus 36-44 2114097-1 1990 S-Adenosylmethionine decarboxylase (AdoMetDC) activity was elevated 18.8-fold in Swiss 3T3 fibroblasts which were depleted of cellular polyamines by using the inhibitor difluoromethylornithine (DFMO). Eflornithine 194-198 adenosylmethionine decarboxylase 1 Rattus norvegicus 0-34 2114097-1 1990 S-Adenosylmethionine decarboxylase (AdoMetDC) activity was elevated 18.8-fold in Swiss 3T3 fibroblasts which were depleted of cellular polyamines by using the inhibitor difluoromethylornithine (DFMO). Eflornithine 194-198 adenosylmethionine decarboxylase 1 Rattus norvegicus 36-44 2114097-6 1990 The shift of the AdoMetDC message into large polysomes occurred within 18 h after addition of DFMO to the cultures and could be reversed by adding exogenous putrescine. Eflornithine 94-98 adenosylmethionine decarboxylase 1 Rattus norvegicus 17-25 6420041-4 1984 Since alpha-difluoromethylornithine (DFMO) and methylglyoxal-bis-guanylhydrazone (MGBG) are irreversible and competitive inhibitors of ODC and SAMDC, respectively, they were tested as single agents and in combination on a transplantable rapidly growing and hormone-resistant G subline of the Dunning R-3327 rat prostatic adenocarcinoma. Eflornithine 37-41 adenosylmethionine decarboxylase 1 Rattus norvegicus 143-148