PubMed:10075645 JSON TXT

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GlyCosmos6-UBERON

{"project":"GlyCosmos6-UBERON","denotations":[{"id":"T1","span":{"begin":128,"end":145},"obj":"Body_part"},{"id":"T2","span":{"begin":162,"end":172},"obj":"Body_part"},{"id":"T3","span":{"begin":260,"end":269},"obj":"Body_part"},{"id":"T5","span":{"begin":271,"end":282},"obj":"Body_part"},{"id":"T6","span":{"begin":288,"end":305},"obj":"Body_part"},{"id":"T7","span":{"begin":707,"end":718},"obj":"Body_part"},{"id":"T8","span":{"begin":719,"end":736},"obj":"Body_part"},{"id":"T9","span":{"begin":1349,"end":1353},"obj":"Body_part"},{"id":"T10","span":{"begin":1354,"end":1361},"obj":"Body_part"},{"id":"T11","span":{"begin":1651,"end":1661},"obj":"Body_part"},{"id":"T12","span":{"begin":1666,"end":1683},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000234"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL_0000576"},{"id":"A4","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL_0001054"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CL_0000235"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_8410081"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CL_0000000"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/UBERON_0002416"},{"id":"A11","pred":"uberon_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CL_0000234"},{"id":"A12","pred":"uberon_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/CL_0000115"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

sentences

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":173},"obj":"Sentence"},{"id":"T2","span":{"begin":174,"end":400},"obj":"Sentence"},{"id":"T3","span":{"begin":401,"end":537},"obj":"Sentence"},{"id":"T4","span":{"begin":538,"end":771},"obj":"Sentence"},{"id":"T5","span":{"begin":772,"end":873},"obj":"Sentence"},{"id":"T6","span":{"begin":874,"end":1079},"obj":"Sentence"},{"id":"T7","span":{"begin":1080,"end":1204},"obj":"Sentence"},{"id":"T8","span":{"begin":1205,"end":1312},"obj":"Sentence"},{"id":"T9","span":{"begin":1313,"end":1387},"obj":"Sentence"},{"id":"T10","span":{"begin":1388,"end":1684},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":115,"end":120},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":367,"end":375},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":384,"end":390},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":694,"end":699},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"NCBItxid:2"},{"id":"A3","pred":"db_id","subj":"T3","obj":"NCBItxid:137507"},{"id":"A4","pred":"db_id","subj":"T4","obj":"NCBItxid:9606"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":612,"end":617},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

GlyCosmos6-CLO

jnlpba-st-training

genia-medco-coref

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":39,"end":60},"obj":"NP"},{"id":"C2","span":{"begin":150,"end":172},"obj":"NP"},{"id":"C3","span":{"begin":288,"end":305},"obj":"NP"},{"id":"C4","span":{"begin":415,"end":424},"obj":"NP"},{"id":"C5","span":{"begin":455,"end":497},"obj":"NP"},{"id":"C6","span":{"begin":499,"end":536},"obj":"NP"},{"id":"C7","span":{"begin":694,"end":770},"obj":"NP"},{"id":"C8","span":{"begin":791,"end":812},"obj":"NP"},{"id":"C10","span":{"begin":1164,"end":1169},"obj":"NP"},{"id":"C9","span":{"begin":1134,"end":1169},"obj":"NP"},{"id":"C11","span":{"begin":1170,"end":1174},"obj":"NP"},{"id":"C12","span":{"begin":1313,"end":1317},"obj":"NP"},{"id":"C13","span":{"begin":1365,"end":1386},"obj":"NP"},{"id":"C14","span":{"begin":1639,"end":1661},"obj":"NP"},{"id":"C15","span":{"begin":1666,"end":1683},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C4","obj":"C1"},{"id":"R2","pred":"coref-appos","subj":"C6","obj":"C5"},{"id":"R3","pred":"coref-ident","subj":"C8","obj":"C7"},{"id":"R4","pred":"coref-relat","subj":"C11","obj":"C9"},{"id":"R5","pred":"coref-ident","subj":"C12","obj":"C10"},{"id":"R6","pred":"coref-ident","subj":"C13","obj":"C8"},{"id":"R7","pred":"coref-ident","subj":"C14","obj":"C2"},{"id":"R8","pred":"coref-ident","subj":"C15","obj":"C3"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

semrep-sample

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":173},"obj":"Sentence"},{"id":"S2","span":{"begin":174,"end":400},"obj":"Sentence"},{"id":"S3","span":{"begin":401,"end":537},"obj":"Sentence"},{"id":"S4","span":{"begin":538,"end":771},"obj":"Sentence"},{"id":"S5","span":{"begin":772,"end":873},"obj":"Sentence"},{"id":"S6","span":{"begin":874,"end":1079},"obj":"Sentence"},{"id":"S7","span":{"begin":1080,"end":1204},"obj":"Sentence"},{"id":"S8","span":{"begin":1205,"end":1312},"obj":"Sentence"},{"id":"S9","span":{"begin":1313,"end":1387},"obj":"Sentence"},{"id":"S10","span":{"begin":1388,"end":1684},"obj":"Sentence"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}

GENIAcorpus

metamap-sample

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":384,"end":390},"obj":"HP_0100806"},{"id":"T2","span":{"begin":612,"end":617},"obj":"HP_0002664"}],"text":"Bacterial lipopolysaccharide activates nuclear factor-kappaB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes.\nBacterial lipopolysaccharide (LPS)-mediated immune responses, including activation of monocytes, macrophages, and endothelial cells, play an important role in the pathogenesis of Gram-negative bacteria-induced sepsis syndrome. Activation of NF-kappaB is thought to be required for cytokine release from LPS-responsive cells, a critical step for endotoxic effects. Here we investigated the role and involvement of interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) signal transducer molecules in LPS signaling in human dermal microvessel endothelial cells (HDMEC) and THP-1 monocytic cells. LPS stimulation of HDMEC and THP-1 cells initiated an IL-1 receptor-like NF-kappaB signaling cascade. In transient cotransfection experiments, dominant negative mutants of the IL-1 signaling pathway, including MyD88, IRAK, IRAK2, and TRAF6 inhibited both IL-1- and LPS-induced NF-kappaB-luciferase activity. LPS-induced NF-kappaB activation was not inhibited by a dominant negative mutant of TRAF2 that is involved in TNF signaling. LPS-induced activation of NF-kappaB-responsive reporter gene was not inhibited by IL-1 receptor antagonist. TLR2 and TLR4 were expressed on the cell surface of HDMEC and THP-1 cells. These findings suggest that a signal transduction molecule in the LPS receptor complex may belong to the IL-1 receptor/toll-like receptor (TLR) super family, and the LPS signaling cascade uses an analogous molecular framework for signaling as IL-1 in mononuclear phagocytes and endothelial cells."}