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is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

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is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

{"project":"GO-BP","denotations":[{"id":"T16690","span":{"begin":543,"end":561},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T16689","span":{"begin":519,"end":553},"obj":"http://purl.obolibrary.org/obo/GO_1901224"},{"id":"T16688","span":{"begin":856,"end":873},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T16687","span":{"begin":624,"end":640},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T16686","span":{"begin":416,"end":432},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T16685","span":{"begin":984,"end":994},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T16684","span":{"begin":543,"end":553},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T16683","span":{"begin":233,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T16682","span":{"begin":120,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0016874"},{"id":"T16681","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0034450"},{"id":"T16680","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_1904667"},{"id":"T16679","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0061630"},{"id":"T16678","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_1904668"},{"id":"T16677","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_1990757"},{"id":"T16676","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_1904666"},{"id":"T16675","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0050372"},{"id":"T16674","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0004842"}],"text":"TRAF1 is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

{"project":"GO-MF","denotations":[{"id":"T16699","span":{"begin":951,"end":974},"obj":"http://purl.obolibrary.org/obo/GO_0005102"},{"id":"T16698","span":{"begin":951,"end":958},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T16697","span":{"begin":120,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0016874"},{"id":"T16696","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0034450"},{"id":"T16695","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0061630"},{"id":"T16694","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_1990757"},{"id":"T16693","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0050372"},{"id":"T16692","span":{"begin":110,"end":135},"obj":"http://purl.obolibrary.org/obo/GO_0004842"},{"id":"T16691","span":{"begin":110,"end":119},"obj":"http://purl.obolibrary.org/obo/GO_0031386"}],"text":"TRAF1 is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

{"project":"GO-CC","denotations":[{"id":"T16703","span":{"begin":810,"end":815},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16702","span":{"begin":668,"end":673},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16701","span":{"begin":452,"end":457},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16700","span":{"begin":291,"end":295},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"TRAF1 is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

{"project":"sentences","denotations":[{"id":"T16375","span":{"begin":1422,"end":1528},"obj":"Sentence"},{"id":"T16374","span":{"begin":1338,"end":1421},"obj":"Sentence"},{"id":"T16373","span":{"begin":1088,"end":1337},"obj":"Sentence"},{"id":"T16372","span":{"begin":1005,"end":1087},"obj":"Sentence"},{"id":"T16371","span":{"begin":892,"end":1004},"obj":"Sentence"},{"id":"T16370","span":{"begin":817,"end":891},"obj":"Sentence"},{"id":"T16369","span":{"begin":642,"end":816},"obj":"Sentence"},{"id":"T16368","span":{"begin":563,"end":641},"obj":"Sentence"},{"id":"T16367","span":{"begin":434,"end":562},"obj":"Sentence"},{"id":"T16366","span":{"begin":327,"end":433},"obj":"Sentence"},{"id":"T16365","span":{"begin":137,"end":326},"obj":"Sentence"},{"id":"T16364","span":{"begin":0,"end":136},"obj":"Sentence"},{"id":"T161","span":{"begin":0,"end":136},"obj":"Sentence"},{"id":"T162","span":{"begin":137,"end":326},"obj":"Sentence"},{"id":"T163","span":{"begin":327,"end":433},"obj":"Sentence"},{"id":"T164","span":{"begin":434,"end":562},"obj":"Sentence"},{"id":"T165","span":{"begin":563,"end":641},"obj":"Sentence"},{"id":"T166","span":{"begin":642,"end":816},"obj":"Sentence"},{"id":"T167","span":{"begin":817,"end":891},"obj":"Sentence"},{"id":"T168","span":{"begin":892,"end":1004},"obj":"Sentence"},{"id":"T169","span":{"begin":1005,"end":1087},"obj":"Sentence"},{"id":"T170","span":{"begin":1088,"end":1337},"obj":"Sentence"},{"id":"T171","span":{"begin":1338,"end":1421},"obj":"Sentence"},{"id":"T172","span":{"begin":1422,"end":1528},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"TRAF1 is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

{"project":"simple1","denotations":[{"id":"T16745","span":{"begin":1502,"end":1507},"obj":"Protein"},{"id":"T16744","span":{"begin":1369,"end":1374},"obj":"Protein"},{"id":"T16743","span":{"begin":1267,"end":1272},"obj":"Protein"},{"id":"T16742","span":{"begin":1040,"end":1043},"obj":"Protein"},{"id":"T16741","span":{"begin":1020,"end":1025},"obj":"Protein"},{"id":"T16740","span":{"begin":907,"end":912},"obj":"Protein"},{"id":"T16739","span":{"begin":840,"end":845},"obj":"Protein"},{"id":"T16738","span":{"begin":738,"end":743},"obj":"Protein"},{"id":"T16737","span":{"begin":642,"end":647},"obj":"Protein"},{"id":"T16736","span":{"begin":611,"end":615},"obj":"Protein"},{"id":"T16735","span":{"begin":563,"end":568},"obj":"Protein"},{"id":"T16734","span":{"begin":482,"end":485},"obj":"Protein"},{"id":"T16733","span":{"begin":434,"end":439},"obj":"Protein"},{"id":"T16732","span":{"begin":404,"end":407},"obj":"Protein"},{"id":"T16731","span":{"begin":389,"end":394},"obj":"Protein"},{"id":"T16730","span":{"begin":363,"end":366},"obj":"Protein"},{"id":"T16729","span":{"begin":341,"end":346},"obj":"Protein"},{"id":"T16728","span":{"begin":174,"end":179},"obj":"Protein"},{"id":"T16727","span":{"begin":110,"end":119},"obj":"Protein"},{"id":"T16726","span":{"begin":0,"end":5},"obj":"Protein"}],"text":"TRAF1 is a unique member of the TRAF protein family because it lacks a RING finger domain and therefore lacks ubiquitin ligase activity. Accumulating data support a role for TRAF1 as both a negative and a positive modulator of NF-κB signalling by certain TNF family receptors, possibly in a cell-type-dependent manner [71,72]. Expression of TRAF1 is inducible by TNF and overexpression of TRAF1 inhibits TNF-induced NF-κB activation. TRAF1-deficient T cells are hyper-responsive to TNF, with enhanced proliferation and activation of the NF-κB signalling pathway. TRAF1 also functions as a negative regulator of CD40-induced NF-κB activation. TRAF1-deficient dendritic cells, however, show attenuated responses to secondary stimulation by TRAF2-dependent factors, suggesting a positive regulatory role in these cells. The mechanism by which TRAF1 modulates NF- κB activation is still unclear. Most probably, TRAF1 competes with TRAF family members for binding to the receptor or other signalling proteins. Alternatively, TRAF1 might recruit A20 with which it can physically interact [73]. A genome-wide association study examining more than 300,000 SNPs among approximately 1,500 autoantibody-positive RA cases and 1,800 controls identified a genetic variation at the TRAF1-complement component 5 locus as an important RA risk locus [74]. Subsequent work indicates that TRAF1 is more likely to be the causative locus [75]. Recent work in a Korean population also demonstrates genetic association of the TRAF1 region with RA [76]."}

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