PMC:3218875 / 30218-32809 JSON TXT

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testone

bionlp-st-ge-2016-spacy-parsed

DLUT931

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T18508","span":{"begin":2357,"end":2361},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T18507","span":{"begin":1045,"end":1050},"obj":"http://www.uniprot.org/uniprot/Q16552"},{"id":"T18506","span":{"begin":1036,"end":1039},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T18505","span":{"begin":797,"end":801},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T18504","span":{"begin":635,"end":640},"obj":"http://www.uniprot.org/uniprot/Q9Y4K3"},{"id":"T18503","span":{"begin":1462,"end":1465},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T18502","span":{"begin":518,"end":521},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T18501","span":{"begin":511,"end":516},"obj":"http://www.uniprot.org/uniprot/P01584"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

bionlp-st-ge-2016-test-proteins

bionlp-st-ge-2016-coref

{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T17512","span":{"begin":1536,"end":1543},"obj":"Antecedent"},{"id":"T17511","span":{"begin":1700,"end":1705},"obj":"Anaphor"},{"id":"T17510","span":{"begin":372,"end":379},"obj":"Antecedent"},{"id":"T17509","span":{"begin":451,"end":463},"obj":"Anaphor"}],"relations":[{"id":"R11438","pred":"boundBy","subj":"T17509","obj":"T17510"},{"id":"R11439","pred":"boundBy","subj":"T17511","obj":"T17512"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

2_test

{"project":"2_test","denotations":[{"id":"21639951-20098459-4289509","span":{"begin":352,"end":354},"obj":"20098459"},{"id":"21639951-16885212-4289510","span":{"begin":532,"end":534},"obj":"16885212"},{"id":"21639951-17242365-4289511","span":{"begin":535,"end":537},"obj":"17242365"},{"id":"21639951-16885212-4289512","span":{"begin":686,"end":688},"obj":"16885212"},{"id":"21639951-17242365-4289513","span":{"begin":803,"end":805},"obj":"17242365"},{"id":"21639951-17911593-4289514","span":{"begin":806,"end":808},"obj":"17911593"},{"id":"21639951-18383392-4289515","span":{"begin":924,"end":926},"obj":"18383392"},{"id":"21639951-18438844-4289516","span":{"begin":927,"end":929},"obj":"18438844"},{"id":"21639951-18759964-4289517","span":{"begin":997,"end":999},"obj":"18759964"},{"id":"21639951-20459811-4289518","span":{"begin":1087,"end":1089},"obj":"20459811"},{"id":"21639951-20870441-4289519","span":{"begin":1227,"end":1229},"obj":"20870441"},{"id":"21639951-18383392-4289520","span":{"begin":1418,"end":1420},"obj":"18383392"},{"id":"21639951-17463289-4289521","span":{"begin":1519,"end":1521},"obj":"17463289"},{"id":"21639951-20470394-4289522","span":{"begin":1835,"end":1837},"obj":"20470394"},{"id":"21639951-19404929-4289523","span":{"begin":2247,"end":2249},"obj":"19404929"},{"id":"21639951-21279994-4289524","span":{"begin":2406,"end":2408},"obj":"21279994"},{"id":"21639951-18759964-4289525","span":{"begin":2581,"end":2583},"obj":"18759964"},{"id":"21639951-20470394-4289526","span":{"begin":2584,"end":2586},"obj":"20470394"},{"id":"21639951-19931339-4289527","span":{"begin":2587,"end":2589},"obj":"19931339"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

pmc-enju-pas

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T17435","span":{"begin":957,"end":962},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T17434","span":{"begin":1392,"end":1398},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T17433","span":{"begin":916,"end":922},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

GO-BP

GO-MF

{"project":"GO-MF","denotations":[{"id":"T18006","span":{"begin":2357,"end":2361},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T18005","span":{"begin":2351,"end":2359},"obj":"http://purl.obolibrary.org/obo/GO_0005149"},{"id":"T18004","span":{"begin":1045,"end":1050},"obj":"http://purl.obolibrary.org/obo/GO_0030367"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T18008","span":{"begin":1063,"end":1068},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T18007","span":{"begin":975,"end":980},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"microRNAs\nmiRNAs are recently discovered regulators of gene expression and represent a class of noncoding RNA molecules essential in many cellular and developmental processes, including immune responses and inflammation. They bind the 3'-UTR of target mRNAs leading to the repression of protein expression and the promotion of target mRNA degradation [77].\nmiR-146a/b and miR-155 are of particular interest for inflammatory signalling to NF-κB, since these miRNAs can be induced by inflammatory stimuli such as IL-1β, TNF and TLRs [78,79]. In addition, miR-146a is an NF-κB-dependent gene, and the NF-κB signalling molecules IRAK1 and TRAF6 were identified as target genes of miR-146a [78] (Figure 1). Similarly, miR-155 was shown to target transcripts for the NF-κB signalling molecules IKKε and RIP1 [79,80]. Notably, both miR-146 and miR-155 are expressed at higher levels in RA synovial fibroblasts and synovial tissue [81,82], as well as in peripheral blood mononuclear cells of RA patients [83]. miR-146a is also overexpressed in CD4+ and IL-17-producing T cells from RA patients [84,85]. Interestingly, a polymorphism in the 3'-UTR of the miR-146a target gene was recently shown to be associated with RA susceptibility [86]. miR-155 overexpression in synovial fibroblasts was able to prevent the TLR and cytokine-inducible expression of specific matrix metalloproteinases that mediate tissue destruction in RA [81]. Moreover, miR-155 was shown to promote TNF production, a key process in the pathogenesis of RA [87]. miR-146 and miR-155 may therefore be important negative regulators of inflammation in RA and their potential for the development of new treatments is substantial. In addition, their increased expression in RA patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy [88], but this will require confirmation using a large and well-defined cohort.\nBesides miR-146 and miR-155, a number of other miRNAs with a potential role in the control of NF-κB-dependent inflammatory responses in RA pathology were recently identified. In this context, miR-124a - a key regulator of the chemokine monocyte chemoattractant protein 1 - was shown to be decreased in synoviocytes from RA patients [89]. Similarly, elevated levels of miR-203 - leading to increased secretion of matrix metalloproteinase-1 and IL-6 - were detected in RA synovial fibroblasts [90]. Finally, miR-16, miR-132, and miR-223 were also shown to have an altered expression in RA patients, indicating their potential as diagnostic biomarkers for pathogenesis [83,88,91]."}

sentences

simple1

BioNLP16_DUT

BioNLP16_Messiy

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-test-tees

test3

PMC:3218875 / 30218-32809 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:3218875 / 30218-32809 JSON TXT