PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25811377-9	2015	Decreased expression of PDI and QSOX1 (p<0.05) reveal an impaired disulfide bond formation pathway, which may underlie nicotine-induced ER stress.	Nicotine	122-130	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	24-27	
28681937-0	2017	Maternal nicotine exposure leads to decreased cardiac protein disulfide isomerase and impaired mitochondrial function in male rat offspring.	Nicotine	9-17	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	54-81	
28681937-5	2017	Recently, our laboratory demonstrated that nicotine impairs placental protein disulfide isomerase (PDI) triggering an increase in endoplasmic reticulum stress, leading us to hypothesize that this may also occur in the heart.	Nicotine	43-51	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	70-97	
28681937-5	2017	Recently, our laboratory demonstrated that nicotine impairs placental protein disulfide isomerase (PDI) triggering an increase in endoplasmic reticulum stress, leading us to hypothesize that this may also occur in the heart.	Nicotine	43-51	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	99-102	
28681937-6	2017	At 3 months of age, nicotine-exposed offspring had 45% decreased PDI levels in the absence of endoplasmic reticulum stress.	Nicotine	20-28	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	65-68	
28681937-8	2017	Collectively, this study suggests that perinatal nicotine exposure decreases PDI, which can promote oxidative damage and mitochondrial damage, associated with a premature decline in cardiac function.	Nicotine	49-57	prolyl 4-hydroxylase subunit beta	Rattus norvegicus	77-80