PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12796402-7 2003 The ectopically expressed hMLH1 protein restored a MMR-proficient phenotype in the hMLH1(+) transfectants, showing a significantly increased and prolonged G(2)-M arrest followed by cell death after 6-TG exposure, compared with the vector controls. Thioguanine 198-202 mutL homolog 1 Homo sapiens 26-31 10213489-6 1999 In contrast to the well-characterized, marked increase in cytotoxicity (> 1 log cell kill) found with 6-thioguanine exposures in HCT116/3-6 (hMLH1+) cells compared to HCT116 (hMLH1-) cells, we found only modest cytotoxicity (10-20% cell kill) in both cell lines when treated with IdUrd or BrdUrd for 1 population doubling. Thioguanine 105-118 mutL homolog 1 Homo sapiens 144-149 9973196-4 1999 Expression of hMLH1 restored normal levels of mPMS2 protein, reduced spontaneous base substitution and microsatellite mutations, increased sensitivity to the toxic effects of 6-thioguanine (6-TG), and restored 6-TG-induced cell cycle arrest. Thioguanine 175-188 mutL homolog 1 Homo sapiens 14-19 9973196-4 1999 Expression of hMLH1 restored normal levels of mPMS2 protein, reduced spontaneous base substitution and microsatellite mutations, increased sensitivity to the toxic effects of 6-thioguanine (6-TG), and restored 6-TG-induced cell cycle arrest. Thioguanine 190-194 mutL homolog 1 Homo sapiens 14-19 9973196-4 1999 Expression of hMLH1 restored normal levels of mPMS2 protein, reduced spontaneous base substitution and microsatellite mutations, increased sensitivity to the toxic effects of 6-thioguanine (6-TG), and restored 6-TG-induced cell cycle arrest. Thioguanine 210-214 mutL homolog 1 Homo sapiens 14-19 9973196-5 1999 Our studies confirm that hMLH1 has an essential role in the maintenance of genomic stability and the potentiation of 6-TG cytotoxicity and provide a system for detailed structure/function analysis of the hMLH1 protein. Thioguanine 117-121 mutL homolog 1 Homo sapiens 25-30 9485033-1 1998 A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure was suggested previously. Thioguanine 144-157 mutL homolog 1 Homo sapiens 15-32 9485033-1 1998 A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure was suggested previously. Thioguanine 144-157 mutL homolog 1 Homo sapiens 34-38 9485033-1 1998 A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure was suggested previously. Thioguanine 159-163 mutL homolog 1 Homo sapiens 15-32 9485033-1 1998 A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure was suggested previously. Thioguanine 159-163 mutL homolog 1 Homo sapiens 34-38 9485033-5 1998 MMR-deficient HCT116 cells or embryonic fibroblasts from MLH1 knockout mice also demonstrated classic DNA damage tolerance responses after 6-TG exposure. Thioguanine 139-143 mutL homolog 1 Homo sapiens 57-61 9233776-6 1997 Furthermore, cisplatin and doxorubicin-resistant ovarian lines deficient in hMLH1 expression are cross-resistant to 6-thioguanine and the methylating agent N-methyl-N-nitrosourea (MNU). Thioguanine 116-129 mutL homolog 1 Homo sapiens 76-81 30770470-5 2019 The deacetylation mimetic mutant, but not the WT and the acetylation mimetic mutant, of MLH1 confers resistance to 6-thioguanine. Thioguanine 115-128 mutL homolog 1 Homo sapiens 88-92 21205838-6 2011 This sensitivity is almost completely rescued by the deletion of Mlh1, which suggests that HR is involved in the repair of the 6-thioG-induced recombinogenic lesions generated by MMR. Thioguanine 127-134 mutL homolog 1 Homo sapiens 65-69 20864418-7 2010 Furthermore, cells expressing these MLH1 mutations exhibited resistance to the MMR-dependent cytotoxic effect of 6-thioguanine (6-TG). Thioguanine 113-126 mutL homolog 1 Homo sapiens 36-40 20864418-7 2010 Furthermore, cells expressing these MLH1 mutations exhibited resistance to the MMR-dependent cytotoxic effect of 6-thioguanine (6-TG). Thioguanine 128-132 mutL homolog 1 Homo sapiens 36-40 20368736-4 2010 We found that BNIP3 protein levels are upregulated in a MLH1 (MMR(+))-dependent manner following 6-TG and 5-FU treatment. Thioguanine 97-101 mutL homolog 1 Homo sapiens 56-60 19603033-6 2009 In addition, the presence of wild-type hMLH1 or hMLH1 re-expression significantly increased sensitivity to 6-thioguanine, a MMR-dependent agent. Thioguanine 107-120 mutL homolog 1 Homo sapiens 39-44 19603033-6 2009 In addition, the presence of wild-type hMLH1 or hMLH1 re-expression significantly increased sensitivity to 6-thioguanine, a MMR-dependent agent. Thioguanine 107-120 mutL homolog 1 Homo sapiens 48-53 19603033-7 2009 Cell-death response to 6-thioguanine and cisplatin was associated with significant proteolysis of MLH1, with XIAP destabilisation and increased caspase-3 activity. Thioguanine 23-36 mutL homolog 1 Homo sapiens 98-102 17426439-4 2007 Our results show that MMR proteins (MLH1 or MSH2) are required for signaling to the autophagic pathway after exposure to 6-TG. Thioguanine 121-125 mutL homolog 1 Homo sapiens 36-40 17616687-8 2007 Interestingly, ATR and Chk1 siRNA transfection in BRCA1-positive cells shows similar levels of 6-TG cytotoxicity as the control transfectant, whereas MSH2 and MLH1 siRNA transfectants show 6-TG resistance as expected. Thioguanine 189-193 mutL homolog 1 Homo sapiens 159-163