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PMC:7556165 / 58547-58888 JSONTXT

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LitCovid-sample-sentences

Id Subject Object Predicate Lexical cue
T357 0-341 Sentence denotes An interesting speculation which could reconcile the two position comes from the hypothesis that while ACE2 is for sure the entry door for the virus, once the infection has evolved, there is the subsequent downregulation of ACE2, responsible for the precipitating of respiratory distress, as showed also in animal models (Kuba et al., 2005).

LitCovid-sample-Pubtator

Id Subject Object Predicate Lexical cue pubann:denotes
1612 103-107 Gene denotes ACE2 Gene:59272
1613 224-228 Gene denotes ACE2 Gene:59272
1616 159-168 Disease denotes infection MESH:D007239
1617 267-287 Disease denotes respiratory distress MESH:D012128

LitCovid-sample-UniProt

Id Subject Object Predicate Lexical cue uniprot_id
T5767 103-107 Protein denotes ACE2 https://www.uniprot.org/uniprot/Q9UFZ6
T5768 224-228 Protein denotes ACE2 https://www.uniprot.org/uniprot/Q9UFZ6

LitCovid-sample-PD-IDO

Id Subject Object Predicate Lexical cue
T224 143-148 http://purl.obolibrary.org/obo/NCBITaxon_10239 denotes virus
T225 159-168 http://purl.obolibrary.org/obo/IDO_0000586 denotes infection

LitCovid-sample-PD-MONDO

Id Subject Object Predicate Lexical cue mondo_id
T337 159-168 Disease denotes infection http://purl.obolibrary.org/obo/MONDO_0005550

LitCovid-sample-PD-HP

Id Subject Object Predicate Lexical cue hp_id
T59 267-287 Phenotype denotes respiratory distress http://purl.obolibrary.org/obo/HP_0002098

LitCovid-PD-HP

Id Subject Object Predicate Lexical cue hp_id
T62 267-287 Phenotype denotes respiratory distress http://purl.obolibrary.org/obo/HP_0002098

LitCovid-PubTator

Id Subject Object Predicate Lexical cue tao:has_database_id
1612 103-107 Gene denotes ACE2 Gene:59272
1613 224-228 Gene denotes ACE2 Gene:59272
1616 159-168 Disease denotes infection MESH:D007239
1617 267-287 Disease denotes respiratory distress MESH:D012128

LitCovid-sentences

Id Subject Object Predicate Lexical cue
T357 0-341 Sentence denotes An interesting speculation which could reconcile the two position comes from the hypothesis that while ACE2 is for sure the entry door for the virus, once the infection has evolved, there is the subsequent downregulation of ACE2, responsible for the precipitating of respiratory distress, as showed also in animal models (Kuba et al., 2005).