PMC:7335494 / 59294-60243 JSON TXT

Annnotations TAB JSON ListView MergeView

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T643","span":{"begin":181,"end":184},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T644","span":{"begin":185,"end":186},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T645","span":{"begin":280,"end":290},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T646","span":{"begin":335,"end":336},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T647","span":{"begin":482,"end":483},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T648","span":{"begin":484,"end":494},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T649","span":{"begin":498,"end":499},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T650","span":{"begin":572,"end":574},"obj":"http://purl.obolibrary.org/obo/UBERON_0003064"},{"id":"T651","span":{"begin":704,"end":714},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T652","span":{"begin":723,"end":724},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T653","span":{"begin":745,"end":746},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T654","span":{"begin":780,"end":790},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T655","span":{"begin":813,"end":821},"obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"T656","span":{"begin":822,"end":832},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T657","span":{"begin":840,"end":841},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T658","span":{"begin":915,"end":925},"obj":"http://purl.obolibrary.org/obo/SO_0000418"}],"text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 2015)."}

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T199","span":{"begin":299,"end":321},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T200","span":{"begin":704,"end":714},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T201","span":{"begin":915,"end":933},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T202","span":{"begin":915,"end":925},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 2015)."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T335","span":{"begin":0,"end":163},"obj":"Sentence"},{"id":"T336","span":{"begin":164,"end":269},"obj":"Sentence"},{"id":"T337","span":{"begin":270,"end":428},"obj":"Sentence"},{"id":"T338","span":{"begin":429,"end":582},"obj":"Sentence"},{"id":"T339","span":{"begin":583,"end":949},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 2015)."}

MyTest

{"project":"MyTest","denotations":[{"id":"32640331-15664804-30720928","span":{"begin":157,"end":161},"obj":"15664804"},{"id":"32640331-25149823-30720929","span":{"begin":263,"end":267},"obj":"25149823"},{"id":"32640331-22542696-30720930","span":{"begin":576,"end":580},"obj":"22542696"},{"id":"32640331-25149823-30720931","span":{"begin":943,"end":947},"obj":"25149823"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 2015)."}

2_test

{"project":"2_test","denotations":[{"id":"32640331-15664804-30720928","span":{"begin":157,"end":161},"obj":"15664804"},{"id":"32640331-25149823-30720929","span":{"begin":263,"end":267},"obj":"25149823"},{"id":"32640331-22542696-30720930","span":{"begin":576,"end":580},"obj":"22542696"},{"id":"32640331-25149823-30720931","span":{"begin":943,"end":947},"obj":"25149823"}],"text":"DHA and EPA are weaker agonists of PPAR-γ (EC50 ~ 10–100 μM), while their oxidized metabolites (such as protectin D1) are much more potent (Yamamoto et al., 2005). Also, ALA or ARA has a similar potency to DHA or EPA for on PPAR-γ, and higher for PPAR-α (Calder, 2015). As PPAR-γ activation reduces inflammatory responses, via the NF-κB pathway, this mechanism could partially explain the anti-inflammatory effects of n-3 PUFAs. Furthermore, n-3 PUFAs were reported to suppress NF-κB activation in a PPAR-γ-independent manner by binding to TLR-4 under certain conditions (Im, 2012). Taking into account all these reports, it looks like three mechanisms are employed by n-3 PUFAs to suppress inflammatory signalling via NF-κB: (1) preventing NF-κB nuclear translocation via PPAR-γ activation, (2) interfering with membrane activation of NF-κB via TLR4 and (3) interaction with GPR120 initiating an anti-inflammatory signalling cascade (Calder, 2015)."}