> top > docs > PubMed:15788408 > annotations

PubMed:15788408 JSONTXT

Annnotations TAB JSON ListView MergeView

sentences

Id Subject Object Predicate Lexical cue
T1 0-127 Sentence denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism.
T2 128-348 Sentence denotes Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss.
T3 349-542 Sentence denotes Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases.
T4 543-652 Sentence denotes Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism.
T5 653-831 Sentence denotes Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4.
T6 832-995 Sentence denotes Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite.
T7 996-1124 Sentence denotes We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct.
T8 1125-1212 Sentence denotes Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels.
T9 1213-1301 Sentence denotes Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment.
T10 1302-1448 Sentence denotes Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter.
T11 1449-1614 Sentence denotes A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment.
T12 1615-1830 Sentence denotes In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression.
T13 1831-1933 Sentence denotes Thus, arsenite-induced up-regulation of VEGF gene transcription occurs by an ATF4-dependent mechanism.

bionlp-st-gro-2013-training

Id Subject Object Predicate Lexical cue
T1 4-22 Chemical denotes oxidative stressor
T2 23-31 Chemical denotes arsenite
T4 42-76 Protein denotes vascular endothelial growth factor
T5 77-81 MessengerRNA denotes mRNA
T7 102-106 TranscriptionFactor denotes ATF4
T8 137-144 Tissue denotes retinal
T10 195-199 Protein denotes VEGF
T14 349-365 Stress denotes Oxidative stress
T15 391-405 Tissue denotes retinal tissue
T18 508-512 Protein denotes VEGF
T21 543-551 Chemical denotes Arsenite
T22 570-588 Chemical denotes oxidative stressor
T24 598-602 Protein denotes VEGF
T26 619-629 Protein denotes HIF-1alpha
T27 686-698 AminoAcid denotes homocysteine
T28 703-724 CellComponent denotes endoplasmic reticulum
T29 725-733 Chemical denotes stressor
T31 745-749 Protein denotes VEGF
T34 805-830 TranscriptionFactor denotes transcription factor ATF4
T35 840-844 TranscriptionFactor denotes ATF4
T37 873-889 Stress denotes oxidative stress
T38 912-916 TranscriptionFactor denotes ATF4
T40 952-956 Protein denotes VEGF
T42 986-994 Chemical denotes arsenite
T43 1013-1021 Chemical denotes arsenite
T45 1055-1059 Gene denotes VEGF
T46 1060-1064 MessengerRNA denotes mRNA
T49 1100-1104 Gene denotes VEGF
T50 1105-1113 Promoter denotes promoter
T51 1125-1133 Chemical denotes Arsenite
T53 1142-1151 Protein denotes eIF2alpha
T56 1192-1204 TranscriptionFactor denotes ATF4 protein
T58 1237-1241 TranscriptionFactor denotes ATF4
T60 1265-1269 Protein denotes VEGF
T62 1282-1290 Chemical denotes arsenite
T64 1320-1324 TranscriptionFactor denotes ATF4
T66 1356-1360 Gene denotes VEGF
T67 1361-1369 Promoter denotes promoter
T68 1375-1383 Chemical denotes arsenite
T69 1410-1414 TranscriptionFactor denotes ATF4
T71 1439-1447 Promoter denotes promoter
T72 1451-1458 ProteinComplex denotes complex
T73 1470-1474 TranscriptionFactor denotes ATF4
T75 1483-1494 DNARegion denotes DNA element
T76 1523-1527 TranscriptionFactor denotes VEGF
T77 1528-1552 DNARegion denotes transcription start site
T80 1595-1603 Chemical denotes arsenite
T81 1645-1662 Chemical denotes thiol antioxidant
T82 1664-1680 Chemical denotes N-acetylcysteine
T84 1707-1715 Chemical denotes arsenite
T85 1719-1723 Protein denotes VEGF
T89 1792-1801 Protein denotes eIF2alpha
T90 1806-1818 TranscriptionFactor denotes ATF4 protein
T92 1837-1845 Chemical denotes arsenite
T95 1871-1875 Gene denotes VEGF
T97 1908-1912 TranscriptionFactor denotes ATF4
E1 32-41 PositiveRegulation denotes activates
E2 82-95 Transcription denotes transcription
E3 145-155 GeneExpression denotes expression
E4 212-230 CellularProcess denotes neovascularization
E5 267-287 Disease denotes macular degeneration
E6 292-312 Disease denotes diabetic retinopathy
E7 425-445 Disease denotes macular degeneration
E8 450-470 Disease denotes diabetic retinopathy
E9 513-523 GeneExpression denotes expression
E10 533-541 Disease denotes diseases
E11 590-597 PositiveRegulation denotes induces
E12 603-613 GeneExpression denotes expression
E13 735-744 Increase denotes increases
E14 750-763 Transcription denotes transcription
E15 794-804 PositiveRegulation denotes activating
E16 848-857 GeneExpression denotes expressed
E17 942-951 Increase denotes increased
E18 957-970 Transcription denotes transcription
E19 1022-1031 Increase denotes increased
E20 1069-1078 PositiveRegulation denotes activated
E21 1079-1092 Transcription denotes transcription
E22 1134-1141 PositiveRegulation denotes induced
E23 1152-1167 Phosphorylation denotes phosphorylation
E24 1182-1191 Increase denotes increased
E25 1213-1225 NegativeRegulation denotes Inactivation
E26 1250-1260 Decrease denotes diminished
E27 1270-1278 ResponseToChemicalStimulus denotes response
E28 1302-1316 GeneExpression denotes Overexpression
E29 1343-1351 PositiveRegulation denotes activate
E30 1426-1434 PositiveRegulation denotes activate
E31 1475-1480 BindingOfProteinToDNA denotes binds
E32 1558-1578 BindingOfTFToTFBindingSiteOfDNA denotes DNA binding activity
E33 1582-1591 Increase denotes increased
E34 1685-1692 NegativeRegulation denotes inhibit
E35 1724-1734 GeneExpression denotes expression
E36 1765-1772 NegativeRegulation denotes inhibit
E37 1773-1788 Phosphorylation denotes phosphorylation
E38 1819-1829 GeneExpression denotes expression
E39 1846-1853 PositiveRegulation denotes induced
E40 1854-1867 PositiveRegulation denotes up-regulation
E41 1876-1894 Transcription denotes gene transcription
E42 336-347 Disease denotes vision loss
E43 1426-1434 PositiveRegulation denotes activate
E44 1765-1772 NegativeRegulation denotes inhibit
R1 T5 T4 encodes mRNA,vascular endothelial growth factor
R2 E3 T8 locatedIn expression,retinal
R4 T14 T15 locatedIn Oxidative stress,retinal tissue
R6 T45 T46 encodes VEGF,mRNA
R7 T49 T50 hasPart VEGF,promoter
R9 T66 T67 hasPart VEGF,promoter
R10 T72 T73 hasPart complex,ATF4
R12 T2 E1 hasAgent arsenite,activates
R13 E2 E1 hasPatient transcription,activates
R14 T5 E2 hasPatient mRNA,transcription
R15 T10 E3 hasPatient VEGF,expression
R16 T18 E9 hasPatient VEGF,expression
R17 T21 E11 hasAgent Arsenite,induces
R18 E12 E11 hasPatient expression,induces
R19 T24 E12 hasPatient VEGF,expression
R20 T27 E13 hasAgent homocysteine,increases
R21 E14 E13 hasPatient transcription,increases
R22 T31 E14 hasPatient VEGF,transcription
R23 T34 E15 hasPatient transcription factor ATF4,activating
R24 T35 E16 hasPatient ATF4,expressed
R25 T38 E17 hasAgent ATF4,increased
R26 E18 E17 hasPatient transcription,increased
R27 T40 E18 hasPatient VEGF,transcription
R28 T43 E19 hasAgent arsenite,increased
R29 T46 E19 hasPatient mRNA,increased
R30 T43 E20 hasAgent arsenite,activated
R31 E21 E20 hasPatient transcription,activated
R32 T50 E21 hasPatient promoter,transcription
R33 T51 E22 hasAgent Arsenite,induced
R34 E23 E22 hasPatient phosphorylation,induced
R35 T53 E23 hasPatient eIF2alpha,phosphorylation
R36 T56 E24 hasPatient ATF4 protein,increased
R37 T58 E25 hasPatient ATF4,Inactivation
R38 E25 E26 hasAgent Inactivation,diminished
R39 E27 E26 hasPatient response,diminished
R40 T60 E27 hasAgent VEGF,response
R41 T64 E28 hasPatient ATF4,Overexpression
R42 E28 E29 hasAgent Overexpression,activate
R43 T67 E29 hasPatient promoter,activate
R44 T68 E30 hasAgent arsenite,activate
R45 T71 E30 hasPatient promoter,activate
R46 T72 E31 hasAgent complex,binds
R47 T75 E31 hasPatient DNA element,binds
R48 T80 E33 hasAgent arsenite,increased
R49 E32 E33 hasPatient DNA binding activity,increased
R50 T82 E34 hasAgent N-acetylcysteine,inhibit
R51 T84 E34 hasPatient arsenite,inhibit
R52 T85 E35 hasPatient VEGF,expression
R53 T81 E36 hasAgent thiol antioxidant,inhibit
R54 E37 E36 hasPatient phosphorylation,inhibit
R55 T89 E37 hasPatient eIF2alpha,phosphorylation
R56 T90 E38 hasPatient ATF4 protein,expression
R57 T92 E39 hasAgent arsenite,induced
R58 E40 E39 hasPatient up-regulation,induced
R59 T92 E40 hasAgent arsenite,up-regulation
R60 E41 E40 hasPatient gene transcription,up-regulation
R61 T95 E41 hasPatient VEGF,gene transcription
R62 T69 E43 hasAgent ATF4,activate
R63 T71 E43 hasPatient promoter,activate
R64 T81 E44 hasAgent thiol antioxidant,inhibit
R65 E38 E44 hasPatient expression,inhibit

2015-BEL-Sample-2

Id Subject Object Predicate Lexical cue
BEL:20067048 0-1886 tscript(p(MGI:Atf4)) increases r(MGI:Hmox1) denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism. Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss. Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases. Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism. Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4. Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite. We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct. Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels. Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment. Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter. A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment. In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression. Thus, arsenite-induced up-regulation of VEGF gene trans
BEL:20067060 0-1932 tscript(p(MGI:Atf4)) directlyIncreases r(MGI:Vegfa) denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism. Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss. Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases. Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism. Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4. Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite. We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct. Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels. Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment. Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter. A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment. In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression. Thus, arsenite-induced up-regulation of VEGF gene transcription occurs by an ATF4-dependent mechanism
BEL:20067048 0-1886 tscript(p(MGI:Atf4)) increases r(MGI:Hmox1) denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism. Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss. Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases. Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism. Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4. Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite. We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct. Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels. Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment. Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter. A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment. In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression. Thus, arsenite-induced up-regulation of VEGF gene trans
BEL:20067060 0-1932 tscript(p(MGI:Atf4)) directlyIncreases r(MGI:Vegfa) denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism. Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss. Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases. Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism. Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4. Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite. We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct. Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels. Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment. Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter. A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment. In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression. Thus, arsenite-induced up-regulation of VEGF gene transcription occurs by an ATF4-dependent mechanism
BEL:20072722 0-1932 a(CHEBI:thapsigargin) increases bp(GOBP:"response to endoplasmic reticulum stress") denotes The oxidative stressor arsenite activates vascular endothelial growth factor mRNA transcription by an ATF4-dependent mechanism. Aberrant retinal expression of vascular endothelial growth factor (VEGF) leading to neovascularization is a central feature of age-related macular degeneration and diabetic retinopathy, two leading causes of vision loss. Oxidative stress is suggested to occur in retinal tissue during age-related macular degeneration and diabetic retinopathy and is suspected in the mechanism of VEGF expression in these diseases. Arsenite, a thiol-reactive oxidative stressor, induces VEGF expression by a HIF-1alpha-independent mechanism. Previously, we demonstrated that homocysteine, an endoplasmic reticulum stressor, increases VEGF transcription by a mechanism dependent upon activating transcription factor ATF4. Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite. We now show that arsenite increased steady state levels of VEGF mRNA and activated transcription from a VEGF promoter construct. Arsenite induced eIF2alpha phosphorylation, resulting in increased ATF4 protein levels. Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment. Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter. A complex containing ATF4 binds a DNA element at +1767 bp relative to the VEGF transcription start site, and DNA binding activity is increased by arsenite treatment. In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression. Thus, arsenite-induced up-regulation of VEGF gene transcription occurs by an ATF4-dependent mechanism

HP-phenotype

Id Subject Object Predicate Lexical cue hp_id
T1 267-287 Phenotype denotes macular degeneration HP:0000608
T2 301-312 Phenotype denotes retinopathy HP:0000488
T3 336-347 Phenotype denotes vision loss HP:0000572
T4 349-365 Phenotype denotes Oxidative stress HP:0025464
T5 425-445 Phenotype denotes macular degeneration HP:0000608
T6 459-470 Phenotype denotes retinopathy HP:0000488
T7 873-889 Phenotype denotes oxidative stress HP:0025464

mondo_disease

Id Subject Object Predicate Lexical cue mondo_id
T1 255-287 Disease denotes age-related macular degeneration http://purl.obolibrary.org/obo/MONDO_0005150
T2 292-312 Disease denotes diabetic retinopathy http://purl.obolibrary.org/obo/MONDO_0005266
T3 336-347 Disease denotes vision loss http://purl.obolibrary.org/obo/MONDO_0001941
T4 413-445 Disease denotes age-related macular degeneration http://purl.obolibrary.org/obo/MONDO_0005150
T5 450-470 Disease denotes diabetic retinopathy http://purl.obolibrary.org/obo/MONDO_0005266

Anatomy-UBERON

Id Subject Object Predicate Lexical cue uberon_id
T1 399-405 Body_part denotes tissue http://purl.obolibrary.org/obo/UBERON_0000479
T2 715-724 Body_part denotes reticulum http://purl.obolibrary.org/obo/UBERON_0007361