PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27212708-4	2016	This probe, based on the specific reaction between imidazoline-2-thione and OCl(-), displayed a selective fluorescent off/on response to OCl(-) with the various reactive oxygen species in a physiological medium.	Reactive Oxygen Species	161-184	occludin	Mus musculus	76-79	
27212708-4	2016	This probe, based on the specific reaction between imidazoline-2-thione and OCl(-), displayed a selective fluorescent off/on response to OCl(-) with the various reactive oxygen species in a physiological medium.	Reactive Oxygen Species	161-184	occludin	Mus musculus	137-140	
17073820-7	2006	In addition, using microvessel isolations following in vivo ischaemia/reperfusion, we were able to show that the tight junction membrane protein, occludin, is an early and specific target in ROS-mediated microvascular injury.	Reactive Oxygen Species	191-194	occludin	Mus musculus	146-154	
34111662-11	2021	Moreover, it confirmed that inhibition of ROS recovered the expression levels of E-cadherin, Occludin and ZO-1, and ameliorated inflammation and mucus secretion in airway in OVA-induced mice exposed to PM2.5.	Reactive Oxygen Species	42-45	occludin	Mus musculus	93-101	
33636390-6	2021	Our mechanistic studies revealed that abnormal reactive oxygen species (ROS) in mutant SOD1-expressing cells induced occludin phosphorylation, which facilitated the subsequent occludin ubiquitination mediated by the E3 ligase ITCH.	Reactive Oxygen Species	47-70	occludin	Mus musculus	117-125	
33636390-6	2021	Our mechanistic studies revealed that abnormal reactive oxygen species (ROS) in mutant SOD1-expressing cells induced occludin phosphorylation, which facilitated the subsequent occludin ubiquitination mediated by the E3 ligase ITCH.	Reactive Oxygen Species	47-70	occludin	Mus musculus	176-184	
33636390-6	2021	Our mechanistic studies revealed that abnormal reactive oxygen species (ROS) in mutant SOD1-expressing cells induced occludin phosphorylation, which facilitated the subsequent occludin ubiquitination mediated by the E3 ligase ITCH.	Reactive Oxygen Species	72-75	occludin	Mus musculus	117-125	
33636390-6	2021	Our mechanistic studies revealed that abnormal reactive oxygen species (ROS) in mutant SOD1-expressing cells induced occludin phosphorylation, which facilitated the subsequent occludin ubiquitination mediated by the E3 ligase ITCH.	Reactive Oxygen Species	72-75	occludin	Mus musculus	176-184