PubMed:23791840 JSONTXT

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":41,"end":45},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:10095"},{"id":"A2","pred":"db_id","subj":"T1","obj":"NCBItxid:10088"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"T2","span":{"begin":136,"end":146},"obj":"Sentence"},{"id":"T3","span":{"begin":147,"end":256},"obj":"Sentence"},{"id":"T4","span":{"begin":257,"end":309},"obj":"Sentence"},{"id":"T5","span":{"begin":310,"end":323},"obj":"Sentence"},{"id":"T6","span":{"begin":324,"end":883},"obj":"Sentence"},{"id":"T7","span":{"begin":884,"end":892},"obj":"Sentence"},{"id":"T8","span":{"begin":893,"end":1098},"obj":"Sentence"},{"id":"T9","span":{"begin":1099,"end":1168},"obj":"Sentence"},{"id":"T10","span":{"begin":1169,"end":1180},"obj":"Sentence"},{"id":"T11","span":{"begin":1181,"end":1284},"obj":"Sentence"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

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MESH:D016640"}],"namespaces":[{"prefix":"_base","uri":"https://w3id.org/biolink/vocab/"},{"prefix":"MESH","uri":"http://id.nlm.nih.gov/mesh/"},{"prefix":"NCBITaxon","uri":"https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id="},{"prefix":"NCBIGene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"OMIM","uri":"https://www.omim.org/entry/"},{"prefix":"DBSNP","uri":"https://www.ncbi.nlm.nih.gov/snp/"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":114,"end":134},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":235,"end":255},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0016018"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0016018"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

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We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T1","span":{"begin":0,"end":22},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":65,"end":73},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":82,"end":103},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":173,"end":194},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":343,"end":365},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":367,"end":371},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":438,"end":442},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":487,"end":491},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":545,"end":550},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":562,"end":569},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":571,"end":575},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":578,"end":586},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":588,"end":616},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":621,"end":625},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":629,"end":643},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":656,"end":660},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":667,"end":671},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":675,"end":681},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":683,"end":687},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":690,"end":697},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":698,"end":712},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":713,"end":720},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":722,"end":758},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":759,"end":767},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":777,"end":785},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":796,"end":803},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":808,"end":812},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":824,"end":845},"obj":"GeneOrGeneProduct"},{"id":"T29","span":{"begin":847,"end":851},"obj":"GeneOrGeneProduct"},{"id":"T30","span":{"begin":868,"end":872},"obj":"GeneOrGeneProduct"},{"id":"T31","span":{"begin":902,"end":910},"obj":"GeneOrGeneProduct"},{"id":"T32","span":{"begin":949,"end":953},"obj":"GeneOrGeneProduct"},{"id":"T33","span":{"begin":955,"end":963},"obj":"GeneOrGeneProduct"},{"id":"T34","span":{"begin":984,"end":988},"obj":"GeneOrGeneProduct"},{"id":"T35","span":{"begin":993,"end":997},"obj":"GeneOrGeneProduct"},{"id":"T36","span":{"begin":1005,"end":1009},"obj":"GeneOrGeneProduct"},{"id":"T37","span":{"begin":1022,"end":1026},"obj":"GeneOrGeneProduct"},{"id":"T38","span":{"begin":1027,"end":1031},"obj":"GeneOrGeneProduct"},{"id":"T39","span":{"begin":1058,"end":1067},"obj":"GeneOrGeneProduct"},{"id":"T40","span":{"begin":1099,"end":1103},"obj":"GeneOrGeneProduct"},{"id":"T41","span":{"begin":1119,"end":1126},"obj":"GeneOrGeneProduct"},{"id":"T42","span":{"begin":1133,"end":1141},"obj":"GeneOrGeneProduct"},{"id":"T43","span":{"begin":1213,"end":1217},"obj":"GeneOrGeneProduct"},{"id":"T44","span":{"begin":1249,"end":1257},"obj":"GeneOrGeneProduct"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":65,"end":73},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":122},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":123,"end":134},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":235,"end":243},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":244,"end":255},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":463,"end":471},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":902,"end":910},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1133,"end":1141},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1249,"end":1257},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"originalLabel","subj":"T7","obj":"DISEASE"},{"id":"A9","pred":"originalLabel","subj":"T9","obj":"DISEASE"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"DISEASE"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"DISEASE"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"DISEASE"},{"id":"A3","pred":"originalLabel","subj":"T3","obj":"D005315"},{"id":"A8","pred":"originalLabel","subj":"T8","obj":"DISEASE"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"D005315"},{"id":"A6","pred":"originalLabel","subj":"T6","obj":"DISEASE"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":0,"end":22},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":343,"end":365},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":367,"end":371},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":438,"end":442},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":487,"end":491},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":545,"end":550},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":571,"end":575},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":578,"end":586},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":588,"end":616},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":621,"end":625},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":629,"end":643},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":683,"end":687},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":698,"end":712},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":722,"end":758},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":759,"end":767},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":777,"end":805},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":808,"end":812},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":824,"end":845},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":847,"end":851},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":949,"end":953},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":955,"end":963},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":984,"end":988},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":993,"end":997},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1005,"end":1009},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":1022,"end":1026},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":1058,"end":1067},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":1099,"end":1103},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":1213,"end":1217},"obj":"GeneOrGeneProduct"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":65,"end":73},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":134},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":235,"end":255},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":902,"end":910},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":1133,"end":1141},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1249,"end":1257},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005015"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0016018"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0016018"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005015"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005015"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005015"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":56,"end":73},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":122},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":123,"end":134},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":235,"end":243},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":244,"end":255},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":463,"end":471},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":893,"end":910},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1133,"end":1141},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1240,"end":1257},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"ID:","subj":"T7","obj":"DISEASE"},{"id":"A6","pred":"ID:","subj":"T6","obj":"DISEASE"},{"id":"A9","pred":"ID:","subj":"T9","obj":"DISEASE"},{"id":"A2","pred":"ID:","subj":"T2","obj":"DISEASE"},{"id":"A8","pred":"ID:","subj":"T8","obj":"DISEASE"},{"id":"A1","pred":"ID:","subj":"T1","obj":"DISEASE"},{"id":"A5","pred":"ID:","subj":"T5","obj":"D005315"},{"id":"A4","pred":"ID:","subj":"T4","obj":"DISEASE"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D005315"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":56,"end":73},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":122},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":123,"end":134},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":235,"end":243},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":244,"end":255},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":463,"end":471},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":893,"end":910},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1133,"end":1141},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1240,"end":1257},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"#label","subj":"T1","obj":"DISEASE"},{"id":"A4","pred":"#label","subj":"T4","obj":"DISEASE"},{"id":"A8","pred":"#label","subj":"T8","obj":"DISEASE"},{"id":"A6","pred":"#label","subj":"T6","obj":"DISEASE"},{"id":"A7","pred":"#label","subj":"T7","obj":"DISEASE"},{"id":"A5","pred":"#label","subj":"T5","obj":"D005315"},{"id":"A9","pred":"#label","subj":"T9","obj":"DISEASE"},{"id":"A2","pred":"#label","subj":"T2","obj":"DISEASE"},{"id":"A3","pred":"#label","subj":"T3","obj":"D005315"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":0,"end":22},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":343,"end":365},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":367,"end":371},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":438,"end":442},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":487,"end":491},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":644,"end":660},"obj":"ChemicalEntity"},{"id":"T7","span":{"begin":662,"end":665},"obj":"ChemicalEntity"},{"id":"T8","span":{"begin":683,"end":687},"obj":"ChemicalEntity"},{"id":"T9","span":{"begin":722,"end":749},"obj":"ChemicalEntity"},{"id":"T10","span":{"begin":777,"end":785},"obj":"ChemicalEntity"},{"id":"T12","span":{"begin":863,"end":866},"obj":"ChemicalEntity"},{"id":"T13","span":{"begin":993,"end":997},"obj":"ChemicalEntity"},{"id":"T14","span":{"begin":1099,"end":1103},"obj":"ChemicalEntity"},{"id":"T15","span":{"begin":1213,"end":1217},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"D000072105"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D000072105"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D000072105"},{"id":"A4","pred":"ID:","subj":"T4","obj":"D000072105"},{"id":"A5","pred":"ID:","subj":"T5","obj":"D000072105"},{"id":"A6","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_33697"},{"id":"A7","pred":"ID:","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_33697"},{"id":"A8","pred":"ID:","subj":"T8","obj":"http://purl.obolibrary.org/obo/CHEBI_17300"},{"id":"A9","pred":"ID:","subj":"T9","obj":"D019704"},{"id":"A10","pred":"ID:","subj":"T10","obj":"D007294"},{"id":"A11","pred":"ID:","subj":"T10","obj":"http://purl.obolibrary.org/obo/CHEBI_24848"},{"id":"A12","pred":"ID:","subj":"T12","obj":"http://purl.obolibrary.org/obo/CHEBI_33697"},{"id":"A13","pred":"ID:","subj":"T13","obj":"http://purl.obolibrary.org/obo/CHEBI_17300"},{"id":"A14","pred":"ID:","subj":"T14","obj":"D000072105"},{"id":"A15","pred":"ID:","subj":"T15","obj":"D000072105"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":41,"end":45},"obj":"OrganismTaxon"}],"text":"Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

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dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.\nOBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress.\nSTUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing.\nRESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\nCONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo."}

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