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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.
T11 1757-1904 Sentence denotes Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression.
T12 1905-2041 Sentence denotes The existence of parallel inverse signaling implies that the induction of adhesion molecule expression by VEGF is very finely regulated.

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.
T11 1757-1904 Sentence denotes Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression.
T12 1905-2041 Sentence denotes The existence of parallel inverse signaling implies that the induction of adhesion molecule expression by VEGF is very finely regulated.
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.
T11 1757-1904 Sentence denotes Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression.
T12 1905-2041 Sentence denotes The existence of parallel inverse signaling implies that the induction of adhesion molecule expression by VEGF is very finely regulated.

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
BEL:20046078 84-2040 p(HGNC:VEGFA) increases tscript(p(HGNC:RELA)) denotes 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. The existence of parallel inverse signaling implies that the induction of adhesion molecule expression by VEGF is very finely regulated

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