PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14597699-2	2003	Here, we report NADPH oxidase-dependent reactive oxygen species (ROS) production and extracellular regulated kinases 1/2 (ERK1/2) phosphorylation on PrPC stimulation in the 1C11 neuroectodermal precursor, in its neuronal differentiated progenies, and in GT1-7 neurohypothalamic and BW5147 lymphoid cells.	Reactive Oxygen Species	40-63	prion protein	Mus musculus	149-153	
17635996-3	2007	Consistent with the increase in Htt aggregation, PrP(C) depletion caused an decrease in proteasome activity and a decrease in the activities of cellular defense enzymes compared with control cells whereas reactive oxygen species (ROS) increased more than threefold.	Reactive Oxygen Species	230-233	prion protein	Mus musculus	49-55	
17635996-4	2007	Therefore, PrP(C) may protect against Htt toxicity in neuronal cells by increasing cellular defense proteins, decreasing ROS and increasing proteasome activity thereby increasing Htt degradation.	Reactive Oxygen Species	121-124	prion protein	Mus musculus	11-17	
17405922-4	2007	Antibody-mediated ligation of PrP(C) recruits transduction pathways, which involve nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species production and target the extracellular-regulated kinases ERK1/2.	Reactive Oxygen Species	153-176	prion protein	Mus musculus	30-36	
22222374-4	2012	In cultured PrP(C)-knockout astrocytes from mice, the absence of PrP(C) caused an increase in intracellular ROS (reactive oxygen species) generation during the first 3h of H(2)O(2) treatment.	Reactive Oxygen Species	108-111	prion protein	Mus musculus	65-70	
22222374-4	2012	In cultured PrP(C)-knockout astrocytes from mice, the absence of PrP(C) caused an increase in intracellular ROS (reactive oxygen species) generation during the first 3h of H(2)O(2) treatment.	Reactive Oxygen Species	113-136	prion protein	Mus musculus	65-70	
22222374-5	2012	This rapid increase in ROS disrupted the cell cycle in the PrP(C)-knockout astrocytes, which increased the population of cells in the sub-G1 phase when compared with cultured wild-type astrocytes.	Reactive Oxygen Species	23-26	prion protein	Mus musculus	59-64	
14597699-5	2003	These data argue for an ubiquitous function of PrPC in cell-redox homeostasis through ROS production.	Reactive Oxygen Species	86-89	prion protein	Mus musculus	47-51	
14597699-4	2003	In 1C11-derived bioaminergic cells, ROS signaling and ERK1/2 phosphorylation are both controlled by Fyn kinase activation, introducing some specificity in PrPC transduction associated with this neuronal context.	Reactive Oxygen Species	36-39	prion protein	Mus musculus	155-159	
31546771-7	2019	We will also illustrate and discuss past and unpublished results demonstrating that Abeta oligomers perturb Ca2+ homeostasis and cause abnormal mitochondrial accumulation of reactive oxygen species by possibly affecting the PrP-dependent downregulation of Fyn kinase activity.	Reactive Oxygen Species	174-197	prion protein	Mus musculus	224-227	
33673626-0	2021	Fibrinogen Interaction with Astrocyte ICAM-1 and PrPC Results in the Generation of ROS and Neuronal Death.	Reactive Oxygen Species	83-86	prion protein	Mus musculus	49-53	
29723291-9	2018	These results indicate that PrPC has a protective role against lethal infection with IAVs through the Cu-binding OR region by reducing ROS in infected lungs.	Reactive Oxygen Species	135-138	prion protein	Mus musculus	28-32	
30222366-3	2018	We recently found that PrPC has a protective role against infection with influenza A viruses (IAVs) in mice by reducing reactive oxygen species in the lungs after infection with IAVs.	Reactive Oxygen Species	120-143	prion protein	Mus musculus	23-27	
29723291-11	2018	It is thus conceivable that PrPC functions to maintain Cu content and regulate SOD1 through the OR region in lungs, thereby reducing ROS in IAV-infected lungs and eventually protecting them from lethal infection with IAVs.	Reactive Oxygen Species	133-136	prion protein	Mus musculus	28-32