PubMed:11108718 / 0-1903
Annnotations
sentences
Id | Subject | Object | Predicate | Lexical cue |
---|---|---|---|---|
T1 | 0-215 | Sentence | denotes | Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. |
T2 | 216-326 | Sentence | denotes | Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. |
T3 | 327-545 | Sentence | denotes | Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells. |
T4 | 546-650 | Sentence | denotes | VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. |
T5 | 651-1020 | Sentence | denotes | These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-kappaB, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase. |
T6 | 1021-1262 | Sentence | denotes | Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression. |
T7 | 1263-1331 | Sentence | denotes | Gel shift analysis revealed that VEGF stimulated NF-kappaB activity. |
T8 | 1332-1419 | Sentence | denotes | This effect was inhibited by phospholipase C, NF-kappaB, or protein kinase C inhibitor. |
T9 | 1420-1537 | Sentence | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. |
T10 | 1538-1756 | Sentence | denotes | These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. |
Glycosmos6-MAT
Id | Subject | Object | Predicate | Lexical cue |
---|---|---|---|---|
T1 | 522-526 | http://purl.obolibrary.org/obo/MAT_0000037 | denotes | vein |
Inflammaging
Id | Subject | Object | Predicate | Lexical cue |
---|---|---|---|---|
T1 | 0-215 | Sentence | denotes | Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. |
T2 | 216-326 | Sentence | denotes | Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. |
T3 | 327-545 | Sentence | denotes | Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells. |
T4 | 546-650 | Sentence | denotes | VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. |
T5 | 651-1020 | Sentence | denotes | These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-kappaB, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase. |
T6 | 1021-1262 | Sentence | denotes | Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression. |
T7 | 1263-1331 | Sentence | denotes | Gel shift analysis revealed that VEGF stimulated NF-kappaB activity. |
T8 | 1332-1419 | Sentence | denotes | This effect was inhibited by phospholipase C, NF-kappaB, or protein kinase C inhibitor. |
T9 | 1420-1537 | Sentence | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. |
T10 | 1538-1756 | Sentence | denotes | These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. |
T1 | 0-215 | Sentence | denotes | Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. |
T2 | 216-326 | Sentence | denotes | Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. |
T3 | 327-545 | Sentence | denotes | Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells. |
T4 | 546-650 | Sentence | denotes | VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. |
T5 | 651-1020 | Sentence | denotes | These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-kappaB, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase. |
T6 | 1021-1262 | Sentence | denotes | Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression. |
T7 | 1263-1331 | Sentence | denotes | Gel shift analysis revealed that VEGF stimulated NF-kappaB activity. |
T8 | 1332-1419 | Sentence | denotes | This effect was inhibited by phospholipase C, NF-kappaB, or protein kinase C inhibitor. |
T9 | 1420-1537 | Sentence | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. |
T10 | 1538-1756 | Sentence | denotes | These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. |
2015-BEL-Sample-2
Id | Subject | Object | Predicate | Lexical cue |
---|---|---|---|---|
BEL:20043444 | 0-1903 | p(HGNC:INS) decreases p(HGNC:SELE) | denotes | Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells. Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells. VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-kappaB, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase. Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression. Gel shift analysis revealed that VEGF stimulated NF-kappaB activity. This effect was inhibited by phospholipase C, NF-kappaB, or protein kinase C inhibitor. VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activation with PI 3'-kinase-mediated suppression, but was independent of nitric oxide and MEK. Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression |
BEL:20046068 | 1420-1670 | p(HGNC:VEGFA) increases r(HGNC:ICAM1) | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activatio |
BEL:20046070 | 1420-1670 | p(HGNC:VEGFA) increases r(HGNC:SELE) | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activatio |
BEL:20046074 | 1420-1670 | p(HGNC:VEGFA) increases r(HGNC:VCAM1) | denotes | VEGF increased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-kappaB-dependent manner. These results suggest that VEGF-stimulated expression of ICAM-1, VCAM-1, and E-selectin mRNAs was mainly through NF-kappaB activatio |
mondo_disease
Id | Subject | Object | Predicate | Lexical cue | mondo_id |
---|---|---|---|---|---|
T1 | 313-325 | Disease | denotes | inflammation | http://purl.obolibrary.org/obo/MONDO_0021166 |
NCBITAXON
Id | Subject | Object | Predicate | Lexical cue | db_id |
---|---|---|---|---|---|
T1 | 506-511 | OrganismTaxon | denotes | human | 9606 |
Anatomy-UBERON
Id | Subject | Object | Predicate | Lexical cue | uberon_id |
---|---|---|---|---|---|
T1 | 197-214 | Body_part | denotes | endothelial cells | http://purl.obolibrary.org/obo/CL_0000115 |
T2 | 288-305 | Body_part | denotes | endothelial cells | http://purl.obolibrary.org/obo/CL_0000115 |
T3 | 512-526 | Body_part | denotes | umbilical vein | http://purl.obolibrary.org/obo/UBERON_0002066 |
T4 | 527-544 | Body_part | denotes | endothelial cells | http://purl.obolibrary.org/obo/CL_0000115 |
T5 | 940-953 | Body_part | denotes | extracellular | http://purl.obolibrary.org/obo/GO_0005576 |
T6 | 1482-1491 | Body_part | denotes | leukocyte | http://purl.obolibrary.org/obo/CL_0000738 |
Anatomy-MAT
Id | Subject | Object | Predicate | Lexical cue | mat_id |
---|---|---|---|---|---|
T1 | 522-526 | Body_part | denotes | vein | http://purl.obolibrary.org/obo/MAT_0000037 |
Glycosmos15-CL
Id | Subject | Object | Predicate | Lexical cue | cl_id |
---|---|---|---|---|---|
T1 | 197-214 | Cell | denotes | endothelial cells | http://purl.obolibrary.org/obo/CL:0000115 |
T2 | 288-305 | Cell | denotes | endothelial cells | http://purl.obolibrary.org/obo/CL:0000115 |
T3 | 522-544 | Cell | denotes | vein endothelial cells | http://purl.obolibrary.org/obo/CL:0002543 |
T4 | 1110-1115 | Cell | denotes | basal | http://purl.obolibrary.org/obo/CL:0002324 |
T5 | 1225-1230 | Cell | denotes | basal | http://purl.obolibrary.org/obo/CL:0002324 |
T6 | 1482-1491 | Cell | denotes | leukocyte | http://purl.obolibrary.org/obo/CL:0000738 |