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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T59","span":{"begin":517,"end":523},"obj":"Body_part"},{"id":"T60","span":{"begin":1924,"end":1930},"obj":"Body_part"},{"id":"T61","span":{"begin":2038,"end":2044},"obj":"Body_part"},{"id":"T62","span":{"begin":2368,"end":2372},"obj":"Body_part"},{"id":"T63","span":{"begin":2585,"end":2589},"obj":"Body_part"},{"id":"T64","span":{"begin":2594,"end":2598},"obj":"Body_part"},{"id":"T65","span":{"begin":3590,"end":3594},"obj":"Body_part"}],"attributes":[{"id":"A59","pred":"uberon_id","subj":"T59","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A60","pred":"uberon_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/UBERON_0000310"},{"id":"A61","pred":"uberon_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/UBERON_0000310"},{"id":"A62","pred":"uberon_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A63","pred":"uberon_id","subj":"T63","obj":"http://purl.obolibrary.org/obo/UBERON_0000033"},{"id":"A64","pred":"uberon_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/UBERON_0000974"},{"id":"A65","pred":"uberon_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/UBERON_0001970"}],"text":"4.1.7. miR1468-5p\nSudden cardiac death is a major problem amongst the unexplained deaths in COVID-19, and it has been identified that many of those patients suffered from primary myocardial fibrosis (PMF), without any known aetiology. Recently, higher expression of miR-1468-3p was identified as a disease-associated and age-dependent cardiac biomarker, as it promotes cardiac fibrosis and cell senescence, although no difference was noted in the mature form of miR-1468 between healthy and COVID-19-diseased cardiac tissue [101]. TGF-β1 plays a key role in fibrosis-related pathologies including cardiac fibrosis, and, furthermore, miR-1468 activates non-canonical TGF-β1 and MAPKs signalling pathways [101]. Moreover, miR-1468-5p expression has been found to be upregulated in regulatory T cells, which have a significant role in autoimmune disorders, transplant rejection, allergic diseases, and asthma [102]. miR-1468-5p has previously been associated with glioma, where it inhibits growth and cell cycle progression by targeting ribonucleotide reductase large subunit M1 (RRM1), based on a study on patients from the Chinese Glioma Genome Atlas [103]. miR-1468-5 is also linked to progressing hepatocellular carcinoma [104]. Interestingly, in Alzheimer’s disease, miR-1468-5p has been identified to be at lower abundance compared with healthy controls [105]. It has furthermore been identified as a biomarker in late seizure in patients with spontaneous intracerebral haemorrhage [49]. The link between miR-1468-5 in viral infection and other comorbidities will need to be further investigated.\nmiR-129-2-3p, here identified as a common mutated miR, has previously been identified as a regulator in human cancer development and progression [106]. It has been identified as a diagnostic and prognostic biomarker for renal cell carcinoma [107] and a suppressor of serous ovarian cancer [104]. Its upregulation suppresses breast cancer cell proliferation and induces its apoptosis, while downregulation, via hypermethylation, increases breast cancer progression due to BCL2L2 overexpression [107]. It furthermore attenuates cell migration and invasion in renal cell carcinoma by affecting the downregulation of various metastasis-related genes [108]. miR129-2 has been linked to a range of haematological malignancies, including lymphoma [109]. It is also linked to lung adenocarcinoma including regulation of cell proliferation [110], as well as to hepatocellular carcinoma [111]. Interestingly, miR-129-2-3p has been found to be upregulated in human papilloma virus-positive (HPV) head and neck squamous cell carcinoma [112] and in HPV transfected keratinocyte cells [113]. In the light of increasing understanding of the link between SARS-CoV-2 and comorbidities, underlying changes in miR-129-2-3p expression may be of considerable importance.\nA number of KEGG pathways have been strongly linked to the main miRs identified as being related to sequences within the SARS-CoV-2 genomes. These include: “Mucin type O-glycan biosynthesis”, “TGF-β signalling pathway”, “Morphine addiction”, “Metabolism of xenobiotics by cytochrome P450”, “Other types of O-glycan biosynthesis”, “Vitamin digestion and absorption”, “Glycosaminoglycan biosynthesis—heparan sulfate/heparin”, “GABAergic synapse”, “Cytokine-cytokine receptor interaction”, “Signalling pathways regulating pluripotency of stem cells”, “Amphetamine addiction”, “Axon guidance”, “Hippo signalling pathway”, “Prolactin signalling pathway”, “mRNA surveillance pathway”, “Glycosphingolipid biosynthesis—lacto and neolacto series”, “Bile secretion”, “Circadian entrainment”, “N-glycan biosynthesis”, “Mismatch repair”, “Drug metabolism—cytochrome P450”, “Glutamatergic synapse”, “Glycosaminoglycan degradation”, “Antigen processing and presentation”. The relevance of several of these KEGG pathways has been discussed above in direct relation to the various miRs and provides a novel insight into the putative interplay of these pathways and the microRNAs identified in COVID-19, and may also help in furthering understanding of the interplay of miRs, viral infections and comorbidities."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-HP

LitCovid-PD-GO-BP

LitCovid-PD-GlycoEpitope

{"project":"LitCovid-PD-GlycoEpitope","denotations":[{"id":"T8","span":{"begin":3248,"end":3263},"obj":"GlycoEpitope"}],"attributes":[{"id":"A8","pred":"glyco_epitope_db_id","subj":"T8","obj":"http://www.glycoepitope.jp/epitopes/EP0086"}],"text":"4.1.7. miR1468-5p\nSudden cardiac death is a major problem amongst the unexplained deaths in COVID-19, and it has been identified that many of those patients suffered from primary myocardial fibrosis (PMF), without any known aetiology. Recently, higher expression of miR-1468-3p was identified as a disease-associated and age-dependent cardiac biomarker, as it promotes cardiac fibrosis and cell senescence, although no difference was noted in the mature form of miR-1468 between healthy and COVID-19-diseased cardiac tissue [101]. TGF-β1 plays a key role in fibrosis-related pathologies including cardiac fibrosis, and, furthermore, miR-1468 activates non-canonical TGF-β1 and MAPKs signalling pathways [101]. Moreover, miR-1468-5p expression has been found to be upregulated in regulatory T cells, which have a significant role in autoimmune disorders, transplant rejection, allergic diseases, and asthma [102]. miR-1468-5p has previously been associated with glioma, where it inhibits growth and cell cycle progression by targeting ribonucleotide reductase large subunit M1 (RRM1), based on a study on patients from the Chinese Glioma Genome Atlas [103]. miR-1468-5 is also linked to progressing hepatocellular carcinoma [104]. Interestingly, in Alzheimer’s disease, miR-1468-5p has been identified to be at lower abundance compared with healthy controls [105]. It has furthermore been identified as a biomarker in late seizure in patients with spontaneous intracerebral haemorrhage [49]. The link between miR-1468-5 in viral infection and other comorbidities will need to be further investigated.\nmiR-129-2-3p, here identified as a common mutated miR, has previously been identified as a regulator in human cancer development and progression [106]. It has been identified as a diagnostic and prognostic biomarker for renal cell carcinoma [107] and a suppressor of serous ovarian cancer [104]. Its upregulation suppresses breast cancer cell proliferation and induces its apoptosis, while downregulation, via hypermethylation, increases breast cancer progression due to BCL2L2 overexpression [107]. It furthermore attenuates cell migration and invasion in renal cell carcinoma by affecting the downregulation of various metastasis-related genes [108]. miR129-2 has been linked to a range of haematological malignancies, including lymphoma [109]. It is also linked to lung adenocarcinoma including regulation of cell proliferation [110], as well as to hepatocellular carcinoma [111]. Interestingly, miR-129-2-3p has been found to be upregulated in human papilloma virus-positive (HPV) head and neck squamous cell carcinoma [112] and in HPV transfected keratinocyte cells [113]. In the light of increasing understanding of the link between SARS-CoV-2 and comorbidities, underlying changes in miR-129-2-3p expression may be of considerable importance.\nA number of KEGG pathways have been strongly linked to the main miRs identified as being related to sequences within the SARS-CoV-2 genomes. These include: “Mucin type O-glycan biosynthesis”, “TGF-β signalling pathway”, “Morphine addiction”, “Metabolism of xenobiotics by cytochrome P450”, “Other types of O-glycan biosynthesis”, “Vitamin digestion and absorption”, “Glycosaminoglycan biosynthesis—heparan sulfate/heparin”, “GABAergic synapse”, “Cytokine-cytokine receptor interaction”, “Signalling pathways regulating pluripotency of stem cells”, “Amphetamine addiction”, “Axon guidance”, “Hippo signalling pathway”, “Prolactin signalling pathway”, “mRNA surveillance pathway”, “Glycosphingolipid biosynthesis—lacto and neolacto series”, “Bile secretion”, “Circadian entrainment”, “N-glycan biosynthesis”, “Mismatch repair”, “Drug metabolism—cytochrome P450”, “Glutamatergic synapse”, “Glycosaminoglycan degradation”, “Antigen processing and presentation”. The relevance of several of these KEGG pathways has been discussed above in direct relation to the various miRs and provides a novel insight into the putative interplay of these pathways and the microRNAs identified in COVID-19, and may also help in furthering understanding of the interplay of miRs, viral infections and comorbidities."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T274","span":{"begin":0,"end":17},"obj":"Sentence"},{"id":"T275","span":{"begin":18,"end":234},"obj":"Sentence"},{"id":"T276","span":{"begin":235,"end":530},"obj":"Sentence"},{"id":"T277","span":{"begin":531,"end":709},"obj":"Sentence"},{"id":"T278","span":{"begin":710,"end":1229},"obj":"Sentence"},{"id":"T279","span":{"begin":1230,"end":1363},"obj":"Sentence"},{"id":"T280","span":{"begin":1364,"end":1490},"obj":"Sentence"},{"id":"T281","span":{"begin":1491,"end":1599},"obj":"Sentence"},{"id":"T282","span":{"begin":1600,"end":1751},"obj":"Sentence"},{"id":"T283","span":{"begin":1752,"end":1895},"obj":"Sentence"},{"id":"T284","span":{"begin":1896,"end":2099},"obj":"Sentence"},{"id":"T285","span":{"begin":2100,"end":2346},"obj":"Sentence"},{"id":"T286","span":{"begin":2347,"end":2483},"obj":"Sentence"},{"id":"T287","span":{"begin":2484,"end":2677},"obj":"Sentence"},{"id":"T288","span":{"begin":2678,"end":2849},"obj":"Sentence"},{"id":"T289","span":{"begin":2850,"end":2990},"obj":"Sentence"},{"id":"T290","span":{"begin":2991,"end":3807},"obj":"Sentence"},{"id":"T291","span":{"begin":3808,"end":4144},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"4.1.7. miR1468-5p\nSudden cardiac death is a major problem amongst the unexplained deaths in COVID-19, and it has been identified that many of those patients suffered from primary myocardial fibrosis (PMF), without any known aetiology. Recently, higher expression of miR-1468-3p was identified as a disease-associated and age-dependent cardiac biomarker, as it promotes cardiac fibrosis and cell senescence, although no difference was noted in the mature form of miR-1468 between healthy and COVID-19-diseased cardiac tissue [101]. TGF-β1 plays a key role in fibrosis-related pathologies including cardiac fibrosis, and, furthermore, miR-1468 activates non-canonical TGF-β1 and MAPKs signalling pathways [101]. Moreover, miR-1468-5p expression has been found to be upregulated in regulatory T cells, which have a significant role in autoimmune disorders, transplant rejection, allergic diseases, and asthma [102]. miR-1468-5p has previously been associated with glioma, where it inhibits growth and cell cycle progression by targeting ribonucleotide reductase large subunit M1 (RRM1), based on a study on patients from the Chinese Glioma Genome Atlas [103]. miR-1468-5 is also linked to progressing hepatocellular carcinoma [104]. Interestingly, in Alzheimer’s disease, miR-1468-5p has been identified to be at lower abundance compared with healthy controls [105]. It has furthermore been identified as a biomarker in late seizure in patients with spontaneous intracerebral haemorrhage [49]. The link between miR-1468-5 in viral infection and other comorbidities will need to be further investigated.\nmiR-129-2-3p, here identified as a common mutated miR, has previously been identified as a regulator in human cancer development and progression [106]. It has been identified as a diagnostic and prognostic biomarker for renal cell carcinoma [107] and a suppressor of serous ovarian cancer [104]. Its upregulation suppresses breast cancer cell proliferation and induces its apoptosis, while downregulation, via hypermethylation, increases breast cancer progression due to BCL2L2 overexpression [107]. It furthermore attenuates cell migration and invasion in renal cell carcinoma by affecting the downregulation of various metastasis-related genes [108]. miR129-2 has been linked to a range of haematological malignancies, including lymphoma [109]. It is also linked to lung adenocarcinoma including regulation of cell proliferation [110], as well as to hepatocellular carcinoma [111]. Interestingly, miR-129-2-3p has been found to be upregulated in human papilloma virus-positive (HPV) head and neck squamous cell carcinoma [112] and in HPV transfected keratinocyte cells [113]. In the light of increasing understanding of the link between SARS-CoV-2 and comorbidities, underlying changes in miR-129-2-3p expression may be of considerable importance.\nA number of KEGG pathways have been strongly linked to the main miRs identified as being related to sequences within the SARS-CoV-2 genomes. These include: “Mucin type O-glycan biosynthesis”, “TGF-β signalling pathway”, “Morphine addiction”, “Metabolism of xenobiotics by cytochrome P450”, “Other types of O-glycan biosynthesis”, “Vitamin digestion and absorption”, “Glycosaminoglycan biosynthesis—heparan sulfate/heparin”, “GABAergic synapse”, “Cytokine-cytokine receptor interaction”, “Signalling pathways regulating pluripotency of stem cells”, “Amphetamine addiction”, “Axon guidance”, “Hippo signalling pathway”, “Prolactin signalling pathway”, “mRNA surveillance pathway”, “Glycosphingolipid biosynthesis—lacto and neolacto series”, “Bile secretion”, “Circadian entrainment”, “N-glycan biosynthesis”, “Mismatch repair”, “Drug metabolism—cytochrome P450”, “Glutamatergic synapse”, “Glycosaminoglycan degradation”, “Antigen processing and presentation”. The relevance of several of these KEGG pathways has been discussed above in direct relation to the various miRs and provides a novel insight into the putative interplay of these pathways and the microRNAs identified in COVID-19, and may also help in furthering understanding of the interplay of miRs, viral infections and comorbidities."}

2_test

{"project":"2_test","denotations":[{"id":"32512929-29515035-144200781","span":{"begin":525,"end":528},"obj":"29515035"},{"id":"32512929-29515035-144200782","span":{"begin":704,"end":707},"obj":"29515035"},{"id":"32512929-32348937-144200783","span":{"begin":907,"end":910},"obj":"32348937"},{"id":"32512929-28239651-144200784","span":{"begin":1151,"end":1154},"obj":"28239651"},{"id":"32512929-28469953-144200785","span":{"begin":1224,"end":1227},"obj":"28469953"},{"id":"32512929-31949677-144200786","span":{"begin":1358,"end":1361},"obj":"31949677"},{"id":"32512929-18055455-144200787","span":{"begin":1486,"end":1488},"obj":"18055455"},{"id":"32512929-31809862-144200788","span":{"begin":1746,"end":1749},"obj":"31809862"},{"id":"32512929-27802440-144200789","span":{"begin":1842,"end":1845},"obj":"27802440"},{"id":"32512929-28469953-144200790","span":{"begin":1890,"end":1893},"obj":"28469953"},{"id":"32512929-27802440-144200791","span":{"begin":2094,"end":2097},"obj":"27802440"},{"id":"32512929-26935022-144200792","span":{"begin":2247,"end":2250},"obj":"26935022"},{"id":"32512929-24802708-144200793","span":{"begin":2341,"end":2344},"obj":"24802708"},{"id":"32512929-23406679-144200794","span":{"begin":2432,"end":2435},"obj":"23406679"},{"id":"32512929-20404570-144200795","span":{"begin":2478,"end":2481},"obj":"20404570"},{"id":"32512929-23205106-144200796","span":{"begin":2624,"end":2627},"obj":"23205106"},{"id":"32512929-29455435-144200797","span":{"begin":2672,"end":2675},"obj":"29455435"}],"text":"4.1.7. miR1468-5p\nSudden cardiac death is a major problem amongst the unexplained deaths in COVID-19, and it has been identified that many of those patients suffered from primary myocardial fibrosis (PMF), without any known aetiology. Recently, higher expression of miR-1468-3p was identified as a disease-associated and age-dependent cardiac biomarker, as it promotes cardiac fibrosis and cell senescence, although no difference was noted in the mature form of miR-1468 between healthy and COVID-19-diseased cardiac tissue [101]. TGF-β1 plays a key role in fibrosis-related pathologies including cardiac fibrosis, and, furthermore, miR-1468 activates non-canonical TGF-β1 and MAPKs signalling pathways [101]. Moreover, miR-1468-5p expression has been found to be upregulated in regulatory T cells, which have a significant role in autoimmune disorders, transplant rejection, allergic diseases, and asthma [102]. miR-1468-5p has previously been associated with glioma, where it inhibits growth and cell cycle progression by targeting ribonucleotide reductase large subunit M1 (RRM1), based on a study on patients from the Chinese Glioma Genome Atlas [103]. miR-1468-5 is also linked to progressing hepatocellular carcinoma [104]. Interestingly, in Alzheimer’s disease, miR-1468-5p has been identified to be at lower abundance compared with healthy controls [105]. It has furthermore been identified as a biomarker in late seizure in patients with spontaneous intracerebral haemorrhage [49]. The link between miR-1468-5 in viral infection and other comorbidities will need to be further investigated.\nmiR-129-2-3p, here identified as a common mutated miR, has previously been identified as a regulator in human cancer development and progression [106]. It has been identified as a diagnostic and prognostic biomarker for renal cell carcinoma [107] and a suppressor of serous ovarian cancer [104]. Its upregulation suppresses breast cancer cell proliferation and induces its apoptosis, while downregulation, via hypermethylation, increases breast cancer progression due to BCL2L2 overexpression [107]. It furthermore attenuates cell migration and invasion in renal cell carcinoma by affecting the downregulation of various metastasis-related genes [108]. miR129-2 has been linked to a range of haematological malignancies, including lymphoma [109]. It is also linked to lung adenocarcinoma including regulation of cell proliferation [110], as well as to hepatocellular carcinoma [111]. Interestingly, miR-129-2-3p has been found to be upregulated in human papilloma virus-positive (HPV) head and neck squamous cell carcinoma [112] and in HPV transfected keratinocyte cells [113]. In the light of increasing understanding of the link between SARS-CoV-2 and comorbidities, underlying changes in miR-129-2-3p expression may be of considerable importance.\nA number of KEGG pathways have been strongly linked to the main miRs identified as being related to sequences within the SARS-CoV-2 genomes. These include: “Mucin type O-glycan biosynthesis”, “TGF-β signalling pathway”, “Morphine addiction”, “Metabolism of xenobiotics by cytochrome P450”, “Other types of O-glycan biosynthesis”, “Vitamin digestion and absorption”, “Glycosaminoglycan biosynthesis—heparan sulfate/heparin”, “GABAergic synapse”, “Cytokine-cytokine receptor interaction”, “Signalling pathways regulating pluripotency of stem cells”, “Amphetamine addiction”, “Axon guidance”, “Hippo signalling pathway”, “Prolactin signalling pathway”, “mRNA surveillance pathway”, “Glycosphingolipid biosynthesis—lacto and neolacto series”, “Bile secretion”, “Circadian entrainment”, “N-glycan biosynthesis”, “Mismatch repair”, “Drug metabolism—cytochrome P450”, “Glutamatergic synapse”, “Glycosaminoglycan degradation”, “Antigen processing and presentation”. The relevance of several of these KEGG pathways has been discussed above in direct relation to the various miRs and provides a novel insight into the putative interplay of these pathways and the microRNAs identified in COVID-19, and may also help in furthering understanding of the interplay of miRs, viral infections and comorbidities."}

LitCovid-PubTator

PMC:7354481 / 41679-45823 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7354481 / 41679-45823 JSON TXT