| http://purl.uniprot.org/citations/31255283 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31255283 | http://www.w3.org/2000/01/rdf-schema#comment | "Ischemic stroke is one of the leading causes of morbidity and mortality among human worldwide. Unfortunately, cerebral I/R still lacks effective therapeutic targets and strategies. In the study, we found that general control nonderepressible 2 (GCN2) expression was increased following ischemia in the ischemic penumbra in vivo and in vitro. GCN2 suppression using its significant inhibitor, GCN2iB, exhibited a protective role in cerebral I/R injury in mice, as evidenced by the improved neurological deficits and function. GCN2 inhibition with either GCN2iB or genetic knockdown led to significant reduction of pro-apoptotic protein expression, endoplasmic reticulum stress (ERS)-related protein and oxidative stress both in I/R-induced cerebral injury and oxygen-glucose deprivation and reoxygenation (OGD/R) stimulation in N2a cells. OGD/R-triggered apoptosis and ERS were significantly depended on oxidative stress in vitro. In addition, Forkhead box O 3a (FoxO3a), involved in the reactive oxygen species (ROS) production, was increased during OGD/R stimulation-regulated apoptosis and ERS, which could be abrogated by GCN2 suppression. Consistently, FoxO3a-regulated generation of ROS was markedly ameliorated upon GCN2 suppression with GCN2iB. Thereby, our findings indicated that GCN2 suppression alleviated apoptosis and ERS in cerebral ischemia through reducing FoxO3a-dependent ROS production, illustrating that GCN2 could be a promising target for the therapeutic interventions in cerebral ischemic stroke."xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2019.05.181"xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/author | "Tian Y."xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/author | "Shi W.Z."xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/pages | "285-292"xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/title | "GCN2 suppression attenuates cerebral ischemia in mice by reducing apoptosis and endoplasmic reticulum (ER) stress through the blockage of FoxO3a-regulated ROS production."xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://purl.uniprot.org/core/volume | "516"xsd:string |
| http://purl.uniprot.org/citations/31255283 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31255283 |
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