PMC:7781431 / 16585-17106 JSONTXT

{"project":"LitCovid-PubTator","denotations":[{"id":"458","span":{"begin":93,"end":97},"obj":"Gene"},{"id":"459","span":{"begin":98,"end":101},"obj":"Gene"},{"id":"460","span":{"begin":301,"end":311},"obj":"Gene"},{"id":"461","span":{"begin":313,"end":318},"obj":"Gene"},{"id":"462","span":{"begin":411,"end":426},"obj":"Gene"},{"id":"463","span":{"begin":428,"end":431},"obj":"Gene"},{"id":"464","span":{"begin":451,"end":456},"obj":"Gene"},{"id":"465","span":{"begin":25,"end":31},"obj":"Chemical"}],"attributes":[{"id":"A458","pred":"tao:has_database_id","subj":"458","obj":"Gene:2358"},{"id":"A459","pred":"tao:has_database_id","subj":"459","obj":"Gene:84941"},{"id":"A460","pred":"tao:has_database_id","subj":"460","obj":"Gene:301"},{"id":"A461","pred":"tao:has_database_id","subj":"461","obj":"Gene:301"},{"id":"A462","pred":"tao:has_database_id","subj":"462","obj":"Gene:6287"},{"id":"A463","pred":"tao:has_database_id","subj":"463","obj":"Gene:6287"},{"id":"A464","pred":"tao:has_database_id","subj":"464","obj":"Gene:820"},{"id":"A465","pred":"tao:has_database_id","subj":"465","obj":"MESH:D008055"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"Endogenous and exogenous lipids, peptides, and proteins have been shown to bind and activate FPR2/ALX to produce inflammatory and anti-inflammatory effects (Takano et al. 1997; Cooray et al. 2013). Both the LXs and Rvs families, including LXA4, AT-LXA4 (15-epi-LXA4), RvD1, AT-RvD1 (17-epi-RvD1), and Annexin A1 (ANXA1) activate receptors with high potency. On the other hand, endogenous antagonists, including serum amyloid A (SAA) and cathelicidin (LL-37) have been identified (Bozinovski et al. 2012; Wan et al. 2011)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T161","span":{"begin":0,"end":170},"obj":"Sentence"},{"id":"T162","span":{"begin":171,"end":190},"obj":"Sentence"},{"id":"T163","span":{"begin":191,"end":197},"obj":"Sentence"},{"id":"T164","span":{"begin":198,"end":357},"obj":"Sentence"},{"id":"T165","span":{"begin":358,"end":497},"obj":"Sentence"},{"id":"T166","span":{"begin":498,"end":514},"obj":"Sentence"},{"id":"T167","span":{"begin":515,"end":521},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Endogenous and exogenous lipids, peptides, and proteins have been shown to bind and activate FPR2/ALX to produce inflammatory and anti-inflammatory effects (Takano et al. 1997; Cooray et al. 2013). Both the LXs and Rvs families, including LXA4, AT-LXA4 (15-epi-LXA4), RvD1, AT-RvD1 (17-epi-RvD1), and Annexin A1 (ANXA1) activate receptors with high potency. On the other hand, endogenous antagonists, including serum amyloid A (SAA) and cathelicidin (LL-37) have been identified (Bozinovski et al. 2012; Wan et al. 2011)."}