PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31980815-3	2020	Here we show that the NEIL3 and the FA/BRCA pathways are non-epistatic in psoralen-ICL repair.	psoralen A	74-82	nei like DNA glycosylase 3	Homo sapiens	22-27	
31980815-4	2020	The NEIL3 pathway is the major pathway for repairing psoralen-ICL, and the FA/BRCA pathway is only activated when NEIL3 is not present.	psoralen A	53-61	nei like DNA glycosylase 3	Homo sapiens	4-9	
31980815-5	2020	Mechanistically, NEIL3 is recruited to psoralen-ICL in a rapid, PARP-dependent manner.	psoralen A	39-47	nei like DNA glycosylase 3	Homo sapiens	17-22	
31980815-6	2020	Importantly, the NEIL3 pathway repairs psoralen-ICLs without generating double-strand breaks (DSBs), unlike the FA/BRCA pathway.	psoralen A	39-47	nei like DNA glycosylase 3	Homo sapiens	17-22	
31980815-7	2020	In addition, we found that the RUVBL1/2 complex physically interact with NEIL3 and function within the NEIL3 pathway in psoralen-ICL repair.	psoralen A	120-128	nei like DNA glycosylase 3	Homo sapiens	73-78	
31980815-7	2020	In addition, we found that the RUVBL1/2 complex physically interact with NEIL3 and function within the NEIL3 pathway in psoralen-ICL repair.	psoralen A	120-128	nei like DNA glycosylase 3	Homo sapiens	103-108	
31980815-10	2020	Taken together, the NEIL3 pathway is the major pathway to repair psoralen-ICL through a unique DSB-free mechanism in human cells.	psoralen A	65-73	nei like DNA glycosylase 3	Homo sapiens	20-25