PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28886188-3 2017 Previous work demonstrated that mice treated with the alkylating agent methyl methanesulfonate (MMS) undergo cerebellar degeneration in an Aag-dependent manner, whereby increased BER initiation by Aag causes increased tissue damage that is dependent on activation of poly (ADP-ribose) polymerase 1 (Parp1). Methyl Methanesulfonate 71-94 poly (ADP-ribose) polymerase family, member 1 Mus musculus 267-297 28886188-3 2017 Previous work demonstrated that mice treated with the alkylating agent methyl methanesulfonate (MMS) undergo cerebellar degeneration in an Aag-dependent manner, whereby increased BER initiation by Aag causes increased tissue damage that is dependent on activation of poly (ADP-ribose) polymerase 1 (Parp1). Methyl Methanesulfonate 71-94 poly (ADP-ribose) polymerase family, member 1 Mus musculus 299-304 28886188-3 2017 Previous work demonstrated that mice treated with the alkylating agent methyl methanesulfonate (MMS) undergo cerebellar degeneration in an Aag-dependent manner, whereby increased BER initiation by Aag causes increased tissue damage that is dependent on activation of poly (ADP-ribose) polymerase 1 (Parp1). Methyl Methanesulfonate 96-99 poly (ADP-ribose) polymerase family, member 1 Mus musculus 267-297 28886188-3 2017 Previous work demonstrated that mice treated with the alkylating agent methyl methanesulfonate (MMS) undergo cerebellar degeneration in an Aag-dependent manner, whereby increased BER initiation by Aag causes increased tissue damage that is dependent on activation of poly (ADP-ribose) polymerase 1 (Parp1). Methyl Methanesulfonate 96-99 poly (ADP-ribose) polymerase family, member 1 Mus musculus 299-304 27391435-6 2016 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate 159-182 poly (ADP-ribose) polymerase family, member 1 Mus musculus 20-25 27391435-6 2016 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate 184-187 poly (ADP-ribose) polymerase family, member 1 Mus musculus 20-25 27391435-6 2016 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate 184-187 poly (ADP-ribose) polymerase family, member 1 Mus musculus 73-81 27391435-9 2016 Pharmacological Parp inhibition in AagTg mice also resulted in sensitivity to MMS-induced nephrotoxicity. Methyl Methanesulfonate 78-81 poly (ADP-ribose) polymerase family, member 1 Mus musculus 16-20 27391435-10 2016 These findings provide in vivo evidence that Parp1 modulates Aag-dependent MMS-induced nephrotoxicity in a sex-dependent manner and highlight the critical roles that Aag-initiated BER and Parp1 may play in determining the side-effects of chemotherapeutic alkylating agents. Methyl Methanesulfonate 75-78 poly (ADP-ribose) polymerase family, member 1 Mus musculus 45-50 23871146-9 2013 PARP inhibition resulted in very strong MMS sensitization in cells expressing wild-type XRCC1, but this sensitization was much less in cells expressing the C12A mutant. Methyl Methanesulfonate 40-43 poly (ADP-ribose) polymerase family, member 1 Mus musculus 0-4 25541391-5 2015 Endogenous DNA damage can substitute for MMS-induced damage such that BER deficiency as a result of either pol beta- or XRCC1-deletion is associated with sensitivity to PARP inhibitors. Methyl Methanesulfonate 41-44 poly (ADP-ribose) polymerase family, member 1 Mus musculus 169-173 22432057-8 2012 XRCC1tp cells showed increased toxicity to MMS, enhanced MMS-induced depletion of NADH suggesting increased PARP activity, and normal functional repair of MMS-induced DNA damage. Methyl Methanesulfonate 57-60 poly (ADP-ribose) polymerase family, member 1 Mus musculus 108-112 22246237-6 2012 These results have implications for explaining the extreme hypersensitivity phenotype after combination treatment with MMS and a PARP inhibitor. Methyl Methanesulfonate 119-122 poly (ADP-ribose) polymerase family, member 1 Mus musculus 129-133 22432057-8 2012 XRCC1tp cells showed increased toxicity to MMS, enhanced MMS-induced depletion of NADH suggesting increased PARP activity, and normal functional repair of MMS-induced DNA damage. Methyl Methanesulfonate 57-60 poly (ADP-ribose) polymerase family, member 1 Mus musculus 108-112 18166976-8 2008 Exposure of wild-type and pol beta(-/-) cells to an inhibitor of PARP activity dramatically potentiates MMS-induced cytotoxicity. Methyl Methanesulfonate 104-107 poly (ADP-ribose) polymerase family, member 1 Mus musculus 65-69 20573551-3 2010 Treatment of human and mouse fibroblasts with the monofunctional DNA methylating agent methyl methanesulfonate (MMS) in the presence of a PARP inhibitor has been shown to trigger a cell cycle checkpoint response. Methyl Methanesulfonate 87-110 poly (ADP-ribose) polymerase family, member 1 Mus musculus 138-142 20573551-3 2010 Treatment of human and mouse fibroblasts with the monofunctional DNA methylating agent methyl methanesulfonate (MMS) in the presence of a PARP inhibitor has been shown to trigger a cell cycle checkpoint response. Methyl Methanesulfonate 112-115 poly (ADP-ribose) polymerase family, member 1 Mus musculus 138-142 20530711-9 2010 After methylmethane sulfonate treatment, PARP inhibition promoted replication-independent accumulation of DSB, repair of which required Ligase IV. Methyl Methanesulfonate 6-29 poly (ADP-ribose) polymerase family, member 1 Mus musculus 41-45 20096707-3 2010 To test the hypothesis that Parp1 is preferentially activated by methyl methanesulfonate (MMS) exposure of Pol beta KO MEFs, we have examined the relationship between Pol beta expression, Parp1 activation and cell survival following MMS exposure in a series of WT and Pol beta deficient MEF cell lines. Methyl Methanesulfonate 65-88 poly (ADP-ribose) polymerase family, member 1 Mus musculus 28-33 20096707-3 2010 To test the hypothesis that Parp1 is preferentially activated by methyl methanesulfonate (MMS) exposure of Pol beta KO MEFs, we have examined the relationship between Pol beta expression, Parp1 activation and cell survival following MMS exposure in a series of WT and Pol beta deficient MEF cell lines. Methyl Methanesulfonate 90-93 poly (ADP-ribose) polymerase family, member 1 Mus musculus 28-33 20096707-5 2010 Both the MMS-induced activation of Parp1 and the MMS-induced cytotoxicity of Pol beta KO MEFs are attenuated by pre-treatment with the Parp1/Parp2 inhibitor PJ34. Methyl Methanesulfonate 9-12 poly (ADP-ribose) polymerase family, member 1 Mus musculus 35-40 20096707-5 2010 Both the MMS-induced activation of Parp1 and the MMS-induced cytotoxicity of Pol beta KO MEFs are attenuated by pre-treatment with the Parp1/Parp2 inhibitor PJ34. Methyl Methanesulfonate 9-12 poly (ADP-ribose) polymerase family, member 1 Mus musculus 135-140 20096707-5 2010 Both the MMS-induced activation of Parp1 and the MMS-induced cytotoxicity of Pol beta KO MEFs are attenuated by pre-treatment with the Parp1/Parp2 inhibitor PJ34. Methyl Methanesulfonate 49-52 poly (ADP-ribose) polymerase family, member 1 Mus musculus 135-140 20096707-8 2010 In addition, the MMS-induced cellular sensitivity of Pol beta KO MEFs is reversed when Parp1 is also deleted (Pol beta/Parp1 double KO MEFs) and we observe no MMS sensitivity differential between Pol beta/Parp1 double KO MEFs and those that express recombinant mouse Pol beta. Methyl Methanesulfonate 17-20 poly (ADP-ribose) polymerase family, member 1 Mus musculus 87-92 20096707-8 2010 In addition, the MMS-induced cellular sensitivity of Pol beta KO MEFs is reversed when Parp1 is also deleted (Pol beta/Parp1 double KO MEFs) and we observe no MMS sensitivity differential between Pol beta/Parp1 double KO MEFs and those that express recombinant mouse Pol beta. Methyl Methanesulfonate 17-20 poly (ADP-ribose) polymerase family, member 1 Mus musculus 119-124 20096707-8 2010 In addition, the MMS-induced cellular sensitivity of Pol beta KO MEFs is reversed when Parp1 is also deleted (Pol beta/Parp1 double KO MEFs) and we observe no MMS sensitivity differential between Pol beta/Parp1 double KO MEFs and those that express recombinant mouse Pol beta. Methyl Methanesulfonate 17-20 poly (ADP-ribose) polymerase family, member 1 Mus musculus 119-124 18691676-1 2008 Inhibition of PARP activity results in extreme sensitization to MMS-induced cell killing in cultured mouse fibroblasts. Methyl Methanesulfonate 64-67 poly (ADP-ribose) polymerase family, member 1 Mus musculus 14-18 18691676-10 2008 Co-immunoprecipitation of PARP-1 and ATR was observed in extracts prepared from MMS-treated cells, but not under conditions of PARP inhibition. Methyl Methanesulfonate 80-83 poly (ADP-ribose) polymerase family, member 1 Mus musculus 26-32 18691676-10 2008 Co-immunoprecipitation of PARP-1 and ATR was observed in extracts prepared from MMS-treated cells, but not under conditions of PARP inhibition. Methyl Methanesulfonate 80-83 poly (ADP-ribose) polymerase family, member 1 Mus musculus 26-30 11752227-8 2002 In an attempt to understand the molecular mechanism of the methyl methanesulfonate (MMS)-induced adaptive response, the present investigations have been undertaken employing nicotinamide, an inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP). Methyl Methanesulfonate 59-82 poly (ADP-ribose) polymerase family, member 1 Mus musculus 226-253 17113833-4 2007 Increased sensitivity to MMS is also seen in the absence of pol beta partner proteins XRCC1 and PARP-1, and under conditions where BER efficiency is reduced by synthetic inhibitors. Methyl Methanesulfonate 25-28 poly (ADP-ribose) polymerase family, member 1 Mus musculus 96-102 17113833-5 2007 PARP activity plays a major role in protection against MMS-induced cytotoxicity, and cells treated with a combination of non-toxic concentrations of MMS and a PARP inhibitor undergo cell cycle arrest and die by a Chk1-dependent apoptotic pathway. Methyl Methanesulfonate 55-58 poly (ADP-ribose) polymerase family, member 1 Mus musculus 0-4 17113833-5 2007 PARP activity plays a major role in protection against MMS-induced cytotoxicity, and cells treated with a combination of non-toxic concentrations of MMS and a PARP inhibitor undergo cell cycle arrest and die by a Chk1-dependent apoptotic pathway. Methyl Methanesulfonate 55-58 poly (ADP-ribose) polymerase family, member 1 Mus musculus 159-163 17113833-5 2007 PARP activity plays a major role in protection against MMS-induced cytotoxicity, and cells treated with a combination of non-toxic concentrations of MMS and a PARP inhibitor undergo cell cycle arrest and die by a Chk1-dependent apoptotic pathway. Methyl Methanesulfonate 149-152 poly (ADP-ribose) polymerase family, member 1 Mus musculus 0-4 16002346-5 2005 We find that inhibition of PARP activity transforms a sub-lethal exposure to MMS into a highly cytotoxic event. Methyl Methanesulfonate 77-80 poly (ADP-ribose) polymerase family, member 1 Mus musculus 27-31 16002346-9 2005 Taken together, our results suggest that inhibition of PARP activity, induced as a result of low dose MMS exposure, signals via a Chk1-dependent pathway for cell death by apoptosis. Methyl Methanesulfonate 102-105 poly (ADP-ribose) polymerase family, member 1 Mus musculus 55-59 15701627-2 2005 Both wild-type and, in particular, repair-deficient DNA polymerase beta null cells are highly sensitized to the cytotoxic effects of MMS by 4-amino-1,8-naphthalimide (4-AN), an inhibitor of poly(ADP-ribose) polymerase (PARP) activity. Methyl Methanesulfonate 133-136 poly (ADP-ribose) polymerase family, member 1 Mus musculus 190-217 15701627-2 2005 Both wild-type and, in particular, repair-deficient DNA polymerase beta null cells are highly sensitized to the cytotoxic effects of MMS by 4-amino-1,8-naphthalimide (4-AN), an inhibitor of poly(ADP-ribose) polymerase (PARP) activity. Methyl Methanesulfonate 133-136 poly (ADP-ribose) polymerase family, member 1 Mus musculus 219-223 15701627-5 2005 In PARP-1-expressing fibroblasts treated with a combination of MMS and 4-AN, a complete inhibition of DNA synthesis is apparent after 4 h, and by 24 h, all cells are arrested in S-phase of the cell cycle. Methyl Methanesulfonate 63-66 poly (ADP-ribose) polymerase family, member 1 Mus musculus 3-9 15701627-8 2005 Our results suggest that inhibition of PARP activity results in sensitization to MMS through maintenance of an ATR and Chk1-dependent S-phase checkpoint. Methyl Methanesulfonate 81-84 poly (ADP-ribose) polymerase family, member 1 Mus musculus 39-43 11752227-8 2002 In an attempt to understand the molecular mechanism of the methyl methanesulfonate (MMS)-induced adaptive response, the present investigations have been undertaken employing nicotinamide, an inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP). Methyl Methanesulfonate 59-82 poly (ADP-ribose) polymerase family, member 1 Mus musculus 255-259 11752227-8 2002 In an attempt to understand the molecular mechanism of the methyl methanesulfonate (MMS)-induced adaptive response, the present investigations have been undertaken employing nicotinamide, an inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP). Methyl Methanesulfonate 84-87 poly (ADP-ribose) polymerase family, member 1 Mus musculus 226-253 11752227-8 2002 In an attempt to understand the molecular mechanism of the methyl methanesulfonate (MMS)-induced adaptive response, the present investigations have been undertaken employing nicotinamide, an inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP). Methyl Methanesulfonate 84-87 poly (ADP-ribose) polymerase family, member 1 Mus musculus 255-259 9592149-4 1998 We found that the lack of PARP renders cells significantly more sensitive to methylmethanesulfonate (MMS), causing cell growth retardation, G2/M accumulation and chromosome instability. Methyl Methanesulfonate 77-99 poly (ADP-ribose) polymerase family, member 1 Mus musculus 26-30 9592149-4 1998 We found that the lack of PARP renders cells significantly more sensitive to methylmethanesulfonate (MMS), causing cell growth retardation, G2/M accumulation and chromosome instability. Methyl Methanesulfonate 101-104 poly (ADP-ribose) polymerase family, member 1 Mus musculus 26-30 9592149-7 1998 Cell viability following MMS treatment could be fully restored after transient expression of the PARP gene. Methyl Methanesulfonate 25-28 poly (ADP-ribose) polymerase family, member 1 Mus musculus 97-101