PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21168393-0	2011	Modulation of Rad51, ERCC1, and thymidine phosphorylase by emodin result in synergistic cytotoxic effect in combination with capecitabine.	Capecitabine	125-137	RAD51 recombinase	Homo sapiens	14-19	
21168393-7	2011	Emodin enhances the capecitabine-induced cytotoxic effects through ERK1/2 inactivation and decreasing the Rad51 and ERCC1 protein levels induced by capecitabine.	Capecitabine	148-160	RAD51 recombinase	Homo sapiens	106-111	
21168393-10	2011	We conclude that enhancing the cytotoxicity to capecitabine by emodin is mediated by down-regulation the expression of Rad51 and ERCC1 and up-regulation TP expression.	Capecitabine	47-59	RAD51 recombinase	Homo sapiens	119-124	
21168393-4	2011	Accordingly, we aimed to explore the molecular mechanism of emodin enhances the capecitabine-induced cytotoxicity through controlling Rad51, ERCC1, and TP expression in human non-small cell lung cancer (NSCLC).	Capecitabine	80-92	RAD51 recombinase	Homo sapiens	134-139	
21168393-5	2011	The results show that capecitabine increases the phosphorylation of MKK1/2-ERK1/2 and protein levels of Rad51 and ERCC1 through enhancing the protein stability.	Capecitabine	22-34	RAD51 recombinase	Homo sapiens	104-109	
21168393-6	2011	Depletion of endogenous Rad51 or ERCC1 expression by specific small interfering RNA transfection significantly increases capecitabine-induced cell death and growth inhibition.	Capecitabine	121-133	RAD51 recombinase	Homo sapiens	24-29