PubMed:12754213
Annnotations
Inflammaging
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T1 | 0-211 | Sentence | denotes | Inhibition of interferon (IFN) gamma-induced Jak-STAT1 activation in microglia by vasoactive intestinal peptide: inhibitory effect on CD40, IFN-induced protein-10, and inducible nitric-oxide synthase expression. |
| T2 | 212-359 | Sentence | denotes | Interferon (IFN)-gamma is one of the most important microglia stimulators in vivo participating in inflammation and Th1 activation/differentiation. |
| T3 | 360-438 | Sentence | denotes | IFN-gamma-mediated signaling involves the activation of the Jak/STAT1 pathway. |
| T4 | 439-684 | Sentence | denotes | The neuropeptides vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase activating polypeptide (PACAP) are two potent microglia-deactivating factors that inhibit the production of proinflammatory mediators in vitro and in vivo. |
| T5 | 685-933 | Sentence | denotes | The present study investigated the molecular mechanisms involved in the VIP/PACAP regulation of several IFN-gamma-induced microglia-derived factors, including IFN-gamma-inducible protein-10 (IP-10), inducible nitric-oxide synthase (iNOS), and CD40. |
| T6 | 934-1205 | Sentence | denotes | The results indicate that VIP/PACAP inhibit Jak1-2 and STAT1 phosphorylation, and the binding of activated STAT1 to the IFN-gamma activated site motif in the IFN regulatory factor-1 and CD40 promoter and to the IFN-stimulated response element motif of the IP-10 promoter. |
| T7 | 1206-1478 | Sentence | denotes | Through its effect in the IFN-gamma-induced Jak/STAT1 pathway, VIP and PACAP are able to control the gene expression of IP-10, CD40, and iNOS, three microglia-derived mediators that play an essential role in several pathologies, i.e. inflammation and autoimmune disorders. |
| T8 | 1479-1604 | Sentence | denotes | The effects of VIP/PACAP are mediated through the specific receptor VPAC1 and the cAMP/protein kinase A transduction pathway. |
| T9 | 1605-1911 | Sentence | denotes | Because IFN-gamma is a major stimulator of innate and adaptive immune responses in vivo, the down-regulation of IFN-gamma-induced gene expression by VIP and PACAP could represent a significant element in the regulation of the inflammatory response in the central nervous system by endogenous neuropeptides. |
| T1 | 0-211 | Sentence | denotes | Inhibition of interferon (IFN) gamma-induced Jak-STAT1 activation in microglia by vasoactive intestinal peptide: inhibitory effect on CD40, IFN-induced protein-10, and inducible nitric-oxide synthase expression. |
| T2 | 212-359 | Sentence | denotes | Interferon (IFN)-gamma is one of the most important microglia stimulators in vivo participating in inflammation and Th1 activation/differentiation. |
| T3 | 360-438 | Sentence | denotes | IFN-gamma-mediated signaling involves the activation of the Jak/STAT1 pathway. |
| T4 | 439-684 | Sentence | denotes | The neuropeptides vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase activating polypeptide (PACAP) are two potent microglia-deactivating factors that inhibit the production of proinflammatory mediators in vitro and in vivo. |
| T5 | 685-933 | Sentence | denotes | The present study investigated the molecular mechanisms involved in the VIP/PACAP regulation of several IFN-gamma-induced microglia-derived factors, including IFN-gamma-inducible protein-10 (IP-10), inducible nitric-oxide synthase (iNOS), and CD40. |
| T6 | 934-1205 | Sentence | denotes | The results indicate that VIP/PACAP inhibit Jak1-2 and STAT1 phosphorylation, and the binding of activated STAT1 to the IFN-gamma activated site motif in the IFN regulatory factor-1 and CD40 promoter and to the IFN-stimulated response element motif of the IP-10 promoter. |
| T7 | 1206-1478 | Sentence | denotes | Through its effect in the IFN-gamma-induced Jak/STAT1 pathway, VIP and PACAP are able to control the gene expression of IP-10, CD40, and iNOS, three microglia-derived mediators that play an essential role in several pathologies, i.e. inflammation and autoimmune disorders. |
| T8 | 1479-1604 | Sentence | denotes | The effects of VIP/PACAP are mediated through the specific receptor VPAC1 and the cAMP/protein kinase A transduction pathway. |
| T9 | 1605-1911 | Sentence | denotes | Because IFN-gamma is a major stimulator of innate and adaptive immune responses in vivo, the down-regulation of IFN-gamma-induced gene expression by VIP and PACAP could represent a significant element in the regulation of the inflammatory response in the central nervous system by endogenous neuropeptides. |
sentences
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T1 | 0-211 | Sentence | denotes | Inhibition of interferon (IFN) gamma-induced Jak-STAT1 activation in microglia by vasoactive intestinal peptide: inhibitory effect on CD40, IFN-induced protein-10, and inducible nitric-oxide synthase expression. |
| T2 | 212-359 | Sentence | denotes | Interferon (IFN)-gamma is one of the most important microglia stimulators in vivo participating in inflammation and Th1 activation/differentiation. |
| T3 | 360-438 | Sentence | denotes | IFN-gamma-mediated signaling involves the activation of the Jak/STAT1 pathway. |
| T4 | 439-684 | Sentence | denotes | The neuropeptides vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase activating polypeptide (PACAP) are two potent microglia-deactivating factors that inhibit the production of proinflammatory mediators in vitro and in vivo. |
| T5 | 685-933 | Sentence | denotes | The present study investigated the molecular mechanisms involved in the VIP/PACAP regulation of several IFN-gamma-induced microglia-derived factors, including IFN-gamma-inducible protein-10 (IP-10), inducible nitric-oxide synthase (iNOS), and CD40. |
| T6 | 934-1205 | Sentence | denotes | The results indicate that VIP/PACAP inhibit Jak1-2 and STAT1 phosphorylation, and the binding of activated STAT1 to the IFN-gamma activated site motif in the IFN regulatory factor-1 and CD40 promoter and to the IFN-stimulated response element motif of the IP-10 promoter. |
| T7 | 1206-1478 | Sentence | denotes | Through its effect in the IFN-gamma-induced Jak/STAT1 pathway, VIP and PACAP are able to control the gene expression of IP-10, CD40, and iNOS, three microglia-derived mediators that play an essential role in several pathologies, i.e. inflammation and autoimmune disorders. |
| T8 | 1479-1604 | Sentence | denotes | The effects of VIP/PACAP are mediated through the specific receptor VPAC1 and the cAMP/protein kinase A transduction pathway. |
| T9 | 1605-1911 | Sentence | denotes | Because IFN-gamma is a major stimulator of innate and adaptive immune responses in vivo, the down-regulation of IFN-gamma-induced gene expression by VIP and PACAP could represent a significant element in the regulation of the inflammatory response in the central nervous system by endogenous neuropeptides. |
Glycosmos6-MAT
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T1 | 93-103 | http://purl.obolibrary.org/obo/MAT_0000043 | denotes | intestinal |
| T2 | 468-478 | http://purl.obolibrary.org/obo/MAT_0000043 | denotes | intestinal |
| T3 | 501-510 | http://purl.obolibrary.org/obo/MAT_0000077 | denotes | pituitary |
| T4 | 1860-1882 | http://purl.obolibrary.org/obo/MAT_0000457 | denotes | central nervous system |
| T5 | 1868-1882 | http://purl.obolibrary.org/obo/MAT_0000026 | denotes | nervous system |
PubMed_ArguminSci
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T1 | 212-359 | DRI_Challenge | denotes | Interferon (IFN)-gamma is one of the most important microglia stimulators in vivo participating in inflammation and Th1 activation/differentiation. |
| T2 | 360-438 | DRI_Approach | denotes | IFN-gamma-mediated signaling involves the activation of the Jak/STAT1 pathway. |
| T3 | 439-684 | DRI_Outcome | denotes | The neuropeptides vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase activating polypeptide (PACAP) are two potent microglia-deactivating factors that inhibit the production of proinflammatory mediators in vitro and in vivo. |
| T4 | 685-788 | DRI_Background | denotes | The present study investigated the molecular mechanisms involved in the VIP/PACAP regulation of several |
| T5 | 825-843 | DRI_Background | denotes | factors, including |
| T6 | 875-933 | DRI_Background | denotes | (IP-10), inducible nitric-oxide synthase (iNOS), and CD40. |
| T7 | 934-1205 | DRI_Outcome | denotes | The results indicate that VIP/PACAP inhibit Jak1-2 and STAT1 phosphorylation, and the binding of activated STAT1 to the IFN-gamma activated site motif in the IFN regulatory factor-1 and CD40 promoter and to the IFN-stimulated response element motif of the IP-10 promoter. |
| T8 | 1206-1231 | DRI_Outcome | denotes | Through its effect in the |
| T9 | 1260-1439 | DRI_Outcome | denotes | pathway, VIP and PACAP are able to control the gene expression of IP-10, CD40, and iNOS, three microglia-derived mediators that play an essential role in several pathologies, i.e. |
| T10 | 1440-1478 | DRI_Background | denotes | inflammation and autoimmune disorders. |
| T11 | 1479-1604 | DRI_Outcome | denotes | The effects of VIP/PACAP are mediated through the specific receptor VPAC1 and the cAMP/protein kinase A transduction pathway. |
| T12 | 1605-1911 | DRI_Background | denotes | Because IFN-gamma is a major stimulator of innate and adaptive immune responses in vivo, the down-regulation of IFN-gamma-induced gene expression by VIP and PACAP could represent a significant element in the regulation of the inflammatory response in the central nervous system by endogenous neuropeptides. |
Anatomy-MAT
| Id | Subject | Object | Predicate | Lexical cue | mat_id |
|---|---|---|---|---|---|
| T1 | 93-103 | Body_part | denotes | intestinal | http://purl.obolibrary.org/obo/MAT_0000043 |
| T2 | 468-478 | Body_part | denotes | intestinal | http://purl.obolibrary.org/obo/MAT_0000043 |
| T3 | 501-510 | Body_part | denotes | pituitary | http://purl.obolibrary.org/obo/MAT_0000077 |
| T4 | 1860-1882 | Body_part | denotes | central nervous system | http://purl.obolibrary.org/obo/MAT_0000457 |
HP-phenotype
| Id | Subject | Object | Predicate | Lexical cue | hp_id |
|---|---|---|---|---|---|
| T1 | 1457-1477 | Phenotype | denotes | autoimmune disorders | HP:0002960 |
mondo_disease
| Id | Subject | Object | Predicate | Lexical cue | mondo_id |
|---|---|---|---|---|---|
| T1 | 311-323 | Disease | denotes | inflammation | http://purl.obolibrary.org/obo/MONDO_0021166 |
| T2 | 501-510 | Disease | denotes | pituitary | http://purl.obolibrary.org/obo/MONDO_0021156 |
| T3 | 1440-1452 | Disease | denotes | inflammation | http://purl.obolibrary.org/obo/MONDO_0021166 |
| T4 | 1457-1477 | Disease | denotes | autoimmune disorders | http://purl.obolibrary.org/obo/MONDO_0007179 |
Anatomy-UBERON
| Id | Subject | Object | Predicate | Lexical cue | uberon_id |
|---|---|---|---|---|---|
| T1 | 501-510 | Body_part | denotes | pituitary | http://purl.obolibrary.org/obo/UBERON_0000007 |
| T2 | 1860-1882 | Body_part | denotes | central nervous system | http://purl.obolibrary.org/obo/UBERON_0001017 |
CL-cell
| Id | Subject | Object | Predicate | Lexical cue | cl_id |
|---|---|---|---|---|---|
| T1 | 55-78 | Cell | denotes | activation in microglia | http://purl.obolibrary.org/obo/CL:0002629 |
| T2 | 69-78 | Cell | denotes | microglia | http://purl.obolibrary.org/obo/CL:0000129 |
| T3 | 264-273 | Cell | denotes | microglia | http://purl.obolibrary.org/obo/CL:0000129 |
| T4 | 575-584 | Cell | denotes | microglia | http://purl.obolibrary.org/obo/CL:0000129 |
| T5 | 807-816 | Cell | denotes | microglia | http://purl.obolibrary.org/obo/CL:0000129 |
| T6 | 1355-1364 | Cell | denotes | microglia | http://purl.obolibrary.org/obo/CL:0000129 |