PubMed:21189258 JSON TXT

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Inflammaging

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":140},"obj":"Sentence"},{"id":"T2","span":{"begin":141,"end":213},"obj":"Sentence"},{"id":"T3","span":{"begin":214,"end":310},"obj":"Sentence"},{"id":"T4","span":{"begin":311,"end":454},"obj":"Sentence"},{"id":"T5","span":{"begin":455,"end":618},"obj":"Sentence"},{"id":"T6","span":{"begin":619,"end":766},"obj":"Sentence"},{"id":"T7","span":{"begin":767,"end":938},"obj":"Sentence"},{"id":"T8","span":{"begin":939,"end":1074},"obj":"Sentence"},{"id":"T9","span":{"begin":1075,"end":1260},"obj":"Sentence"},{"id":"T10","span":{"begin":1261,"end":1376},"obj":"Sentence"},{"id":"T11","span":{"begin":1377,"end":1519},"obj":"Sentence"},{"id":"T12","span":{"begin":1520,"end":1739},"obj":"Sentence"},{"id":"T13","span":{"begin":1740,"end":1875},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":140},"obj":"Sentence"},{"id":"T2","span":{"begin":141,"end":213},"obj":"Sentence"},{"id":"T3","span":{"begin":214,"end":310},"obj":"Sentence"},{"id":"T4","span":{"begin":311,"end":454},"obj":"Sentence"},{"id":"T5","span":{"begin":455,"end":618},"obj":"Sentence"},{"id":"T6","span":{"begin":619,"end":766},"obj":"Sentence"},{"id":"T7","span":{"begin":767,"end":938},"obj":"Sentence"},{"id":"T8","span":{"begin":939,"end":1074},"obj":"Sentence"},{"id":"T9","span":{"begin":1075,"end":1260},"obj":"Sentence"},{"id":"T10","span":{"begin":1261,"end":1376},"obj":"Sentence"},{"id":"T11","span":{"begin":1377,"end":1519},"obj":"Sentence"},{"id":"T12","span":{"begin":1520,"end":1739},"obj":"Sentence"},{"id":"T13","span":{"begin":1740,"end":1875},"obj":"Sentence"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

sentences

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":140},"obj":"Sentence"},{"id":"T2","span":{"begin":141,"end":213},"obj":"Sentence"},{"id":"T3","span":{"begin":214,"end":310},"obj":"Sentence"},{"id":"T4","span":{"begin":311,"end":454},"obj":"Sentence"},{"id":"T5","span":{"begin":455,"end":618},"obj":"Sentence"},{"id":"T6","span":{"begin":619,"end":766},"obj":"Sentence"},{"id":"T7","span":{"begin":767,"end":938},"obj":"Sentence"},{"id":"T8","span":{"begin":939,"end":1074},"obj":"Sentence"},{"id":"T9","span":{"begin":1075,"end":1260},"obj":"Sentence"},{"id":"T10","span":{"begin":1261,"end":1376},"obj":"Sentence"},{"id":"T11","span":{"begin":1377,"end":1519},"obj":"Sentence"},{"id":"T12","span":{"begin":1520,"end":1739},"obj":"Sentence"},{"id":"T13","span":{"begin":1740,"end":1875},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

Glycosmos6-MAT

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":414,"end":420},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

bionlp-st-pc-2013-training

Allie

{"project":"Allie","denotations":[{"id":"SS1_21189258_7_0","span":{"begin":968,"end":995},"obj":"expanded"},{"id":"SS2_21189258_7_0","span":{"begin":997,"end":1003},"obj":"abbr"}],"relations":[{"id":"AE1_21189258_7_0","pred":"abbreviatedTo","subj":"SS1_21189258_7_0","obj":"SS2_21189258_7_0"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":191,"end":203},"obj":"Disease"},{"id":"T2","span":{"begin":271,"end":283},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":408,"end":413},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":835,"end":840},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"9606"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

Anatomy-UBERON

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":414,"end":420},"obj":"Body_part"},{"id":"T2","span":{"begin":429,"end":445},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000066"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

Anatomy-MAT

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":414,"end":420},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000119"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}

CL-cell

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":429,"end":445},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000066"}],"text":"Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.\nTGF-β1 is a pleiotropic cytokine with potent anti-inflammation property. However, the mechanisms underlying TGF-β1 suppression of inflammation remain largely unexplored. In this study, we demonstrated that TGF-β1 inhibited TNF-α- or IL-1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8). To delineate the mechanism by which TGF-β1 inhibits RANTES expression, we examined the potential signal pathway activated by TGF-β1 in suppressing NF-κB signaling. TGF-β1 affected neither TNF-α-induced IκBα phosphorylation and subsequent degradation, nor p65 NF-κB phosphorylation and its nuclear translocation. However, TGF-β1 could inhibit p65 and p50 binding to the κB site in human RANTES promoter as revealed by chromatin immunoprecipitation assay and protein-DNA binding assay. We found that TGF-β1 induced glycogen synthase kinase-3β (GSK-3β) phosphorylation on Ser-9 in HKC-8 cells, leading to its inactivation. Knockdown of GSK-3β mimicked TGF-β1 and inhibited RANTES induction, whereas overexpression of GSK-3β abolished the inhibitory effect of TGF-β1 and completely restored RANTES expression. Furthermore, TGF-β1 induced the dephosphorylation and activation of β-catenin, a major downstream target of GSK-3β. Ectopic expression of constitutively active β-catenin mimicked the TGF-β1 effect and completely suppressed RANTES expression induced by TNF-α. Interestingly, TGF-β1 induced a physical interaction between β-catenin and p65 NF-κB, which prevented p65 binding to the κB site, sequestered its trans-activating activity, and repressed p65-mediated gene transcription. We conclude that TGF-β1 inhibition of proinflammatory RANTES expression is mediated by β-catenin-triggered blockade of NF-κB signaling."}