PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32380118-3 2020 hAAG was titrated using untreated and methyl methanesulfonate (MMS)-treated TK-6 cells. Methyl Methanesulfonate 38-61 N-methylpurine DNA glycosylase Homo sapiens 0-4 32380118-3 2020 hAAG was titrated using untreated and methyl methanesulfonate (MMS)-treated TK-6 cells. Methyl Methanesulfonate 63-66 N-methylpurine DNA glycosylase Homo sapiens 0-4 9708359-2 1998 The amount of AP sites in MMS-treated HeLa cells transiently increased at 3 h, then gradually decreased to 40% at 24 h. The presence of adenine, an inhibitor of AP endonucleases, in the repair incubation of MMS-treated cells induced moderate accumulation of AP sites, suggesting inhibition of the activities of MPG as well as AP endonucleases by adenine metabolites. Methyl Methanesulfonate 26-29 N-methylpurine DNA glycosylase Homo sapiens 311-314 23290262-5 2013 We identify mitochondrial single-stranded binding protein (mtSSB) as a novel interacting partner of AAG; interaction between mtSSB and AAG is direct and increases upon methyl methanesulfonate (MMS) treatment. Methyl Methanesulfonate 168-191 N-methylpurine DNA glycosylase Homo sapiens 100-103 23290262-5 2013 We identify mitochondrial single-stranded binding protein (mtSSB) as a novel interacting partner of AAG; interaction between mtSSB and AAG is direct and increases upon methyl methanesulfonate (MMS) treatment. Methyl Methanesulfonate 168-191 N-methylpurine DNA glycosylase Homo sapiens 135-138 23290262-5 2013 We identify mitochondrial single-stranded binding protein (mtSSB) as a novel interacting partner of AAG; interaction between mtSSB and AAG is direct and increases upon methyl methanesulfonate (MMS) treatment. Methyl Methanesulfonate 193-196 N-methylpurine DNA glycosylase Homo sapiens 100-103 23290262-5 2013 We identify mitochondrial single-stranded binding protein (mtSSB) as a novel interacting partner of AAG; interaction between mtSSB and AAG is direct and increases upon methyl methanesulfonate (MMS) treatment. Methyl Methanesulfonate 193-196 N-methylpurine DNA glycosylase Homo sapiens 135-138 18992265-6 2008 MPG expression remained fairly steady, but in contrast significant up-regulation of MGMT was observed when cells were treated with 0.5 and 1.0 microg/ml MMS for 4h (2.5- and 6.5-fold increases respectively). Methyl Methanesulfonate 153-156 N-methylpurine DNA glycosylase Homo sapiens 0-3 12566303-6 2003 With MPG overexpression, an increase in DNA damage and increased cytotoxicity to methyl methanesulfonate as well as increased apoptosis levels was observed in these cells. Methyl Methanesulfonate 81-104 N-methylpurine DNA glycosylase Homo sapiens 5-8 12566303-8 2003 Overexpression of the mitochondrially targeted MPG dramatically increased the breast cancer cells" sensitivity to methyl methanesulfonate. Methyl Methanesulfonate 114-137 N-methylpurine DNA glycosylase Homo sapiens 47-50 32042007-5 2020 To address this question, we temporally profiled repair and metabolism in wild-type and Aag-/- cells treated with the alkylating agent methyl methanesulfonate (MMS). Methyl Methanesulfonate 135-158 N-methylpurine DNA glycosylase Homo sapiens 88-91 32042007-5 2020 To address this question, we temporally profiled repair and metabolism in wild-type and Aag-/- cells treated with the alkylating agent methyl methanesulfonate (MMS). Methyl Methanesulfonate 160-163 N-methylpurine DNA glycosylase Homo sapiens 88-91 32042007-7 2020 Accordingly, Aag-/- cells are protected from MMS-induced NAD+ depletion and glycolysis inhibition. Methyl Methanesulfonate 45-48 N-methylpurine DNA glycosylase Homo sapiens 13-16 32042007-8 2020 MMS-induced mitochondrial dysfunction, however, is AAG-independent. Methyl Methanesulfonate 0-3 N-methylpurine DNA glycosylase Homo sapiens 51-54 32042007-9 2020 Furthermore, treatment with FK866, a selective inhibitor of the NAD+ salvage pathway enzyme nicotinamide phosphoribosyltransferase (NAMPT), synergizes with MMS to induce cytotoxicity and Aag-/- cells are resistant to this combination FK866 and MMS treatment. Methyl Methanesulfonate 156-159 N-methylpurine DNA glycosylase Homo sapiens 187-190 16288039-6 2005 Two HeLa cell lines with AAG protein levels reduced by at least 80% to 90% displayed a 5- to 10-fold increase in sensitivity to methyl methanesulfonate, N-methyl-N-nitrosourea, and the chemotherapeutic drugs temozolomide and 1,3-bis(2-chloroethyl)-1-nitrosourea. Methyl Methanesulfonate 128-151 N-methylpurine DNA glycosylase Homo sapiens 25-28 16288039-8 2005 After treatment with methyl methanesulfonate, AAG knockdown HeLa cells were delayed in S phase but accumulated in G2-M. Our data support the hypothesis that ablation of AAG activity in human tumor cells may provide a useful strategy to enhance the efficacy of current chemotherapeutic regimens that include alkylating agents. Methyl Methanesulfonate 21-44 N-methylpurine DNA glycosylase Homo sapiens 169-172 15651853-5 2005 The ability of purified wild-type and AAG variants to remove 3-methyladenine and 7-methylguanine, the two most abundant adducts produced by methyl methanesulfonate, was also determined. Methyl Methanesulfonate 140-163 N-methylpurine DNA glycosylase Homo sapiens 38-41 15651853-10 2005 Expression of the N169A and N169S AAG variants in S. cerevisiae during methyl methanesulfonate exposure resulted in greater sensitivity, greater mutation induction following MMS exposure, and more strand breaks in vivo. Methyl Methanesulfonate 71-94 N-methylpurine DNA glycosylase Homo sapiens 34-37 15651853-10 2005 Expression of the N169A and N169S AAG variants in S. cerevisiae during methyl methanesulfonate exposure resulted in greater sensitivity, greater mutation induction following MMS exposure, and more strand breaks in vivo. Methyl Methanesulfonate 174-177 N-methylpurine DNA glycosylase Homo sapiens 34-37 15299078-2 2004 Our results show that MPG-overexpressing cells are significantly more sensitive to the alkylating agents methyl methanesulfonate, N-methyl-N"-nitro-N-nitrosoguanidine, methylnitrosourea, dimethyl sulfate, and the clinical chemotherapeutic temozolomide. Methyl Methanesulfonate 105-128 N-methylpurine DNA glycosylase Homo sapiens 22-25 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 215-237 N-methylpurine DNA glycosylase Homo sapiens 82-85 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 215-237 N-methylpurine DNA glycosylase Homo sapiens 108-111 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 215-237 N-methylpurine DNA glycosylase Homo sapiens 108-111 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 215-237 N-methylpurine DNA glycosylase Homo sapiens 108-111 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 239-242 N-methylpurine DNA glycosylase Homo sapiens 82-85 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 239-242 N-methylpurine DNA glycosylase Homo sapiens 108-111 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 239-242 N-methylpurine DNA glycosylase Homo sapiens 108-111 14555760-4 2003 Chromatin immunoprecipitation analysis reveals the molecular movement of MBD1 and MPG in vivo: (i) The MBD1-MPG complex normally exists on the methylated gene promoter; (ii) treatment of cells with alkylating agent methylmethanesulfonate (MMS) induces the dissociation of MBD1 from the methylated promoter, and MPG is located on both methylated and unmethylated promoters; and (iii) after completion of the repair, the MBD1-MPG complex is restored on the methylated promoter. Methyl Methanesulfonate 239-242 N-methylpurine DNA glycosylase Homo sapiens 108-111 9708359-2 1998 The amount of AP sites in MMS-treated HeLa cells transiently increased at 3 h, then gradually decreased to 40% at 24 h. The presence of adenine, an inhibitor of AP endonucleases, in the repair incubation of MMS-treated cells induced moderate accumulation of AP sites, suggesting inhibition of the activities of MPG as well as AP endonucleases by adenine metabolites. Methyl Methanesulfonate 207-210 N-methylpurine DNA glycosylase Homo sapiens 311-314 35483785-6 2022 In contrast, overexpression of MPG had only a very mild protective effect on the cellular defense against MMS and MNNG. Methyl Methanesulfonate 106-109 N-methylpurine DNA glycosylase Homo sapiens 31-34 1874728-1 1991 A 871-base pair cDNA encoding the human N-methylpurine-DNA glycosylase (MPG) was cloned from a HeLa S3 cDNA expression library in a pUC vector by phenotypic screening of MPG-negative (tag- alkA-) Escherichia coli cells exposed to methylmethane sulfonate. Methyl Methanesulfonate 230-253 N-methylpurine DNA glycosylase Homo sapiens 40-70 1874728-1 1991 A 871-base pair cDNA encoding the human N-methylpurine-DNA glycosylase (MPG) was cloned from a HeLa S3 cDNA expression library in a pUC vector by phenotypic screening of MPG-negative (tag- alkA-) Escherichia coli cells exposed to methylmethane sulfonate. Methyl Methanesulfonate 230-253 N-methylpurine DNA glycosylase Homo sapiens 72-75