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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T164","span":{"begin":106,"end":114},"obj":"Body_part"},{"id":"T165","span":{"begin":144,"end":148},"obj":"Body_part"},{"id":"T166","span":{"begin":156,"end":165},"obj":"Body_part"},{"id":"T167","span":{"begin":446,"end":449},"obj":"Body_part"},{"id":"T168","span":{"begin":712,"end":720},"obj":"Body_part"},{"id":"T169","span":{"begin":1166,"end":1171},"obj":"Body_part"},{"id":"T170","span":{"begin":1363,"end":1372},"obj":"Body_part"},{"id":"T171","span":{"begin":1540,"end":1548},"obj":"Body_part"},{"id":"T172","span":{"begin":1615,"end":1625},"obj":"Body_part"},{"id":"T173","span":{"begin":1648,"end":1659},"obj":"Body_part"},{"id":"T174","span":{"begin":1672,"end":1689},"obj":"Body_part"},{"id":"T175","span":{"begin":1716,"end":1734},"obj":"Body_part"},{"id":"T176","span":{"begin":1743,"end":1747},"obj":"Body_part"}],"attributes":[{"id":"A164","pred":"fma_id","subj":"T164","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A165","pred":"fma_id","subj":"T165","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A166","pred":"fma_id","subj":"T166","obj":"http://purl.org/sig/ont/fma/fma66835"},{"id":"A167","pred":"fma_id","subj":"T167","obj":"http://purl.org/sig/ont/fma/fma67095"},{"id":"A168","pred":"fma_id","subj":"T168","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A169","pred":"fma_id","subj":"T169","obj":"http://purl.org/sig/ont/fma/fma67498"},{"id":"A170","pred":"fma_id","subj":"T170","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A171","pred":"fma_id","subj":"T171","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A172","pred":"fma_id","subj":"T172","obj":"http://purl.org/sig/ont/fma/fma63261"},{"id":"A173","pred":"fma_id","subj":"T173","obj":"http://purl.org/sig/ont/fma/fma62860"},{"id":"A174","pred":"fma_id","subj":"T174","obj":"http://purl.org/sig/ont/fma/fma14704"},{"id":"A175","pred":"fma_id","subj":"T175","obj":"http://purl.org/sig/ont/fma/fma82785"},{"id":"A176","pred":"fma_id","subj":"T176","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T6","span":{"begin":1166,"end":1171},"obj":"Body_part"},{"id":"T7","span":{"begin":1672,"end":1689},"obj":"Body_part"},{"id":"T8","span":{"begin":1743,"end":1747},"obj":"Body_part"}],"attributes":[{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0001179"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T149","span":{"begin":498,"end":507},"obj":"Disease"},{"id":"T150","span":{"begin":635,"end":643},"obj":"Disease"},{"id":"T151","span":{"begin":703,"end":711},"obj":"Disease"},{"id":"T152","span":{"begin":1748,"end":1754},"obj":"Disease"},{"id":"T153","span":{"begin":1774,"end":1809},"obj":"Disease"},{"id":"T154","span":{"begin":1780,"end":1809},"obj":"Disease"}],"attributes":[{"id":"A149","pred":"mondo_id","subj":"T149","obj":"http://purl.obolibrary.org/obo/MONDO_0005812"},{"id":"A150","pred":"mondo_id","subj":"T150","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A151","pred":"mondo_id","subj":"T151","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A152","pred":"mondo_id","subj":"T152","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A153","pred":"mondo_id","subj":"T153","obj":"http://purl.obolibrary.org/obo/MONDO_0006502"},{"id":"A154","pred":"mondo_id","subj":"T154","obj":"http://purl.obolibrary.org/obo/MONDO_0009971"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T597","span":{"begin":106,"end":114},"obj":"Chemical"},{"id":"T598","span":{"begin":124,"end":131},"obj":"Chemical"},{"id":"T599","span":{"begin":266,"end":275},"obj":"Chemical"},{"id":"T600","span":{"begin":305,"end":314},"obj":"Chemical"},{"id":"T601","span":{"begin":370,"end":380},"obj":"Chemical"},{"id":"T602","span":{"begin":712,"end":720},"obj":"Chemical"},{"id":"T603","span":{"begin":765,"end":772},"obj":"Chemical"},{"id":"T604","span":{"begin":963,"end":974},"obj":"Chemical"},{"id":"T605","span":{"begin":1227,"end":1237},"obj":"Chemical"},{"id":"T606","span":{"begin":1562,"end":1564},"obj":"Chemical"},{"id":"T608","span":{"begin":1716,"end":1734},"obj":"Chemical"}],"attributes":[{"id":"A597","pred":"chebi_id","subj":"T597","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A598","pred":"chebi_id","subj":"T598","obj":"http://purl.obolibrary.org/obo/CHEBI_33252"},{"id":"A599","pred":"chebi_id","subj":"T599","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A600","pred":"chebi_id","subj":"T600","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A601","pred":"chebi_id","subj":"T601","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A602","pred":"chebi_id","subj":"T602","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A603","pred":"chebi_id","subj":"T603","obj":"http://purl.obolibrary.org/obo/CHEBI_33252"},{"id":"A604","pred":"chebi_id","subj":"T604","obj":"http://purl.obolibrary.org/obo/CHEBI_22586"},{"id":"A605","pred":"chebi_id","subj":"T605","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A606","pred":"chebi_id","subj":"T606","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A607","pred":"chebi_id","subj":"T606","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A608","pred":"chebi_id","subj":"T608","obj":"http://purl.obolibrary.org/obo/CHEBI_16412"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T58","span":{"begin":228,"end":249},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T59","span":{"begin":228,"end":241},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T60","span":{"begin":823,"end":837},"obj":"http://purl.obolibrary.org/obo/GO_0019068"},{"id":"T61","span":{"begin":917,"end":931},"obj":"http://purl.obolibrary.org/obo/GO_0051168"},{"id":"T62","span":{"begin":1014,"end":1035},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T63","span":{"begin":1014,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T64","span":{"begin":1125,"end":1147},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T65","span":{"begin":1333,"end":1342},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T66","span":{"begin":1540,"end":1558},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T67","span":{"begin":1549,"end":1558},"obj":"http://purl.obolibrary.org/obo/GO_0046903"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T25","span":{"begin":1430,"end":1436},"obj":"Phenotype"},{"id":"T26","span":{"begin":1780,"end":1800},"obj":"Phenotype"}],"attributes":[{"id":"A25","pred":"hp_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/HP_0100806"},{"id":"A26","pred":"hp_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/HP_0002098"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T299","span":{"begin":0,"end":250},"obj":"Sentence"},{"id":"T300","span":{"begin":251,"end":355},"obj":"Sentence"},{"id":"T301","span":{"begin":356,"end":524},"obj":"Sentence"},{"id":"T302","span":{"begin":525,"end":652},"obj":"Sentence"},{"id":"T303","span":{"begin":653,"end":773},"obj":"Sentence"},{"id":"T304","span":{"begin":774,"end":860},"obj":"Sentence"},{"id":"T305","span":{"begin":861,"end":1042},"obj":"Sentence"},{"id":"T306","span":{"begin":1043,"end":1185},"obj":"Sentence"},{"id":"T307","span":{"begin":1186,"end":1396},"obj":"Sentence"},{"id":"T308","span":{"begin":1397,"end":1504},"obj":"Sentence"},{"id":"T309","span":{"begin":1505,"end":1690},"obj":"Sentence"},{"id":"T310","span":{"begin":1691,"end":1816},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Considering the current viral pandemic, CRM1 has been put forward as a facilitator of the export of viral proteins from the nucleus of the host cell to the cytoplasm as well as an amplifier of the activities of pro-inflammatory transcription factors. Thus, the CRM1 inhibitor selinexor may exert relevant antiviral and anti-inflammatory effects [122,123]. In fact, CRM1 inhibitors have exhibited activity against \u003e20 different viruses, including RNA viruses such as respiratory syncytial virus and influenza virus [122,123]. Furthermore, CRM1 inhibition has also been identified in in vitro assays to have a potential activity against SARS-CoV-2 [124]. CRM1 was found to contribute to exporting several SARS-CoV proteins, such as S, N, 9b, Orf3 and Orf6 out of the nucleus. Thus, CRM1 inhibition is expected to inhibit the viral assembly [125,126,127,128,129]. Moreover, CRM1 has also been found to contribute to the nuclear export and functional inactivation of antioxidant, anti-inflammatory, and cytoprotective transcription factors [130]. High levels of CRM1 are found in multiple inflammatory conditions and may magnify inflammatory responses leading to severe organ damage [131]. In this direction, selinexor and similar inhibitors have exhibited potent anti-inflammatory activity by suppressing the activation of NFkB and p38 signaling, leading to reduced cytokines in a variety of models. For example, in a mouse model of sepsis, selinexor increased survival following a lethal dose of endotoxin. Selinexor reduced the inflammatory cytokine secretion of IL-6, TNF-α, and HMGB1 while reducing the numbers of macrophage and polymorphonuclear neutrophils in the mice peritoneal cavity. Selinexor also mitigated lipopolysaccharide-induced lung injury that is similar to acute respiratory distress syndrome [132]."}

LitCovid-PubTator

PMC:7600245 / 39638-41454 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7600245 / 39638-41454 JSON TXT