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