PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25310987-3	2014	Here, we show that Rad5(HLTF/SHPRH), which mediates the error-free branch, has a major role in the response to DNA damage caused by methyl methanesulfonate (MMS) during chromosome replication, whereas translesion synthesis polymerases make only a minor contribution.	Methyl Methanesulfonate	132-155	helicase like transcription factor	Homo sapiens	24-28	
25310987-3	2014	Here, we show that Rad5(HLTF/SHPRH), which mediates the error-free branch, has a major role in the response to DNA damage caused by methyl methanesulfonate (MMS) during chromosome replication, whereas translesion synthesis polymerases make only a minor contribution.	Methyl Methanesulfonate	157-160	helicase like transcription factor	Homo sapiens	24-28	
33281189-0	2020	The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.	Methyl Methanesulfonate	99-122	helicase like transcription factor	Homo sapiens	4-8	
21396873-6	2011	In contrast, MMS promotes the degradation of HLTF and the interactions of SHPRH with Rad18 and polymerase kappa.	Methyl Methanesulfonate	13-16	helicase like transcription factor	Homo sapiens	45-49	
21504827-2	2011	(2011) describe how HLTF and SHPRH, the human homologs of yeast Rad5, can discriminate between MMS-induced versus UV-induced DNA damage.	Methyl Methanesulfonate	95-98	helicase like transcription factor	Homo sapiens	20-24	
33281189-4	2020	The depletion of HLTF and PARP1 increases chromosome breaks, further reduces the length of replication tracks, and concomitantly increases the number of stalled forks after methyl methanesulfonate treatment according to a DNA fiber analysis.	Methyl Methanesulfonate	173-196	helicase like transcription factor	Homo sapiens	17-21	
32192191-2	2020	Here we show that HLTF, SHPRH and HLTF/SHPRH knockout cell lines show different sensitivities towards UV-irradiation, methyl methanesulfonate (MMS), cisplatin and mitomycin C (MMC), which are drugs that induce different types of DNA lesions.	Methyl Methanesulfonate	118-141	helicase like transcription factor	Homo sapiens	18-22	
32192191-2	2020	Here we show that HLTF, SHPRH and HLTF/SHPRH knockout cell lines show different sensitivities towards UV-irradiation, methyl methanesulfonate (MMS), cisplatin and mitomycin C (MMC), which are drugs that induce different types of DNA lesions.	Methyl Methanesulfonate	118-141	helicase like transcription factor	Homo sapiens	34-38	
32192191-2	2020	Here we show that HLTF, SHPRH and HLTF/SHPRH knockout cell lines show different sensitivities towards UV-irradiation, methyl methanesulfonate (MMS), cisplatin and mitomycin C (MMC), which are drugs that induce different types of DNA lesions.	Methyl Methanesulfonate	143-146	helicase like transcription factor	Homo sapiens	18-22	
32192191-2	2020	Here we show that HLTF, SHPRH and HLTF/SHPRH knockout cell lines show different sensitivities towards UV-irradiation, methyl methanesulfonate (MMS), cisplatin and mitomycin C (MMC), which are drugs that induce different types of DNA lesions.	Methyl Methanesulfonate	143-146	helicase like transcription factor	Homo sapiens	34-38	
32192191-3	2020	In general, the HLTF/SHPRH double knockout cell line was less sensitive than the single knockouts in response to all drugs, and interestingly, especially to MMS and cisplatin.	Methyl Methanesulfonate	157-160	helicase like transcription factor	Homo sapiens	16-20	
32192191-4	2020	Using the SupF assay, we detected an increase in the mutation frequency in HLTF knockout cells both after UV- and MMS-induced DNA lesions, while we detected a decrease in mutation frequency over UV lesions in the HLTF/SHPRH double knockout cells.	Methyl Methanesulfonate	114-117	helicase like transcription factor	Homo sapiens	75-79