PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23110144-7	2012	Several active molecules were identified that inhibited APE1 in two independent assay formats and exhibited potentiation of the genotoxic effect of methyl methanesulfonate with a concomitant increase in AP sites, a hallmark of intracellular APE1 inhibition; a number of these chemotypes could be good starting points for further medicinal chemistry optimization.	Methyl Methanesulfonate	148-171	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	56-60	
28181292-4	2017	We report herein that the tumor-associated APE1 variant, R237C, shows reduced complementation efficiency of the methyl methanesulfonate hypersensitivity and impaired cell growth exhibited by APE1-deficient mouse embryonic fibroblasts.	Methyl Methanesulfonate	112-135	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	43-47	
23110144-7	2012	Several active molecules were identified that inhibited APE1 in two independent assay formats and exhibited potentiation of the genotoxic effect of methyl methanesulfonate with a concomitant increase in AP sites, a hallmark of intracellular APE1 inhibition; a number of these chemotypes could be good starting points for further medicinal chemistry optimization.	Methyl Methanesulfonate	148-171	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	241-245	
20808930-7	2010	Expression of the APE1 mutants deficient in the NIR and exonuclease activities reduced the sensitivity of AP endonuclease-deficient E. coli xth nfo strain to an alkylating agent, methylmethanesulfonate, suggesting that our APE1 mutants are able to repair AP sites.	Methyl Methanesulfonate	179-201	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	18-22	
20808930-7	2010	Expression of the APE1 mutants deficient in the NIR and exonuclease activities reduced the sensitivity of AP endonuclease-deficient E. coli xth nfo strain to an alkylating agent, methylmethanesulfonate, suggesting that our APE1 mutants are able to repair AP sites.	Methyl Methanesulfonate	179-201	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	223-227	
15210853-10	2004	A decrease in APE1 levels in siRNA-treated human osteogenic sarcoma cells led to enhanced cell sensitization to the DNA damaging agents: methyl methanesulfonate, H(2)O(2), ionizing radiation, and chemotherapeutic agents.	Methyl Methanesulfonate	137-160	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	14-18	
18776186-5	2008	Interestingly, GAPDH-small interfering RNA knockdown sensitized the cells to methyl methane sulfonate and bleomycin, which generate lesions that are repaired by APE1, but showed normal sensitivity to 254-nm UV.	Methyl Methanesulfonate	77-101	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	161-165	
8559661-6	1995	High-level Ape expression corresponding to approximately 7000 molecules per nucleus, equal to the normal Apn1 copy number, restored resistance to methyl methanesulfonate to near wild-type levels in Apn1-deficient (apn1-) yeast.	Methyl Methanesulfonate	146-169	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	11-14	
8592168-3	1995	The cell lines having lower APEX expression showed higher sensitivity to MMS and H2O2 which are known to induce AP sites and single strand breaks on DNA, respectively.	Methyl Methanesulfonate	73-76	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	28-32