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several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"DLUT931","denotations":[{"id":"T11919","span":{"begin":977,"end":986},"obj":"Negative_regulation"},{"id":"T11918","span":{"begin":991,"end":1004},"obj":"Transcription"},{"id":"T11917","span":{"begin":745,"end":751},"obj":"Regulation"},{"id":"T11916","span":{"begin":243,"end":252},"obj":"Negative_regulation"},{"id":"T11915","span":{"begin":223,"end":234},"obj":"Binding"},{"id":"T11895","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T11894","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T11893","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T11892","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T11891","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T11890","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T11889","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T11888","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T11887","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T11886","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T11885","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T11884","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T11883","span":{"begin":39,"end":42},"obj":"Protein"}],"relations":[{"id":"R8102","pred":"themeOf","subj":"T11884","obj":"T11915"},{"id":"R8103","pred":"themeOf","subj":"T11884","obj":"T11916"},{"id":"R8108","pred":"themeOf","subj":"T11892","obj":"T11917"},{"id":"R8109","pred":"themeOf","subj":"T11894","obj":"T11918"},{"id":"R8120","pred":"themeOf","subj":"T11915","obj":"T11916"},{"id":"R8122","pred":"themeOf","subj":"T11918","obj":"T11919"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T11727","span":{"begin":608,"end":611},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T11726","span":{"begin":583,"end":586},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T11718","span":{"begin":987,"end":990},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11717","span":{"begin":939,"end":942},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11716","span":{"begin":759,"end":762},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11715","span":{"begin":678,"end":681},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11714","span":{"begin":548,"end":551},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11713","span":{"begin":461,"end":464},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11712","span":{"begin":414,"end":417},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11711","span":{"begin":260,"end":263},"obj":"http://www.uniprot.org/uniprot/P21580"},{"id":"T11710","span":{"begin":39,"end":42},"obj":"http://www.uniprot.org/uniprot/P21580"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

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several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"GO-BP","denotations":[{"id":"T10682","span":{"begin":991,"end":1004},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T10681","span":{"begin":103,"end":114},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T10634","span":{"begin":595,"end":602},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"GO-CC","denotations":[{"id":"T10734","span":{"begin":282,"end":292},"obj":"http://purl.obolibrary.org/obo/GO_0005694"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"sentences","denotations":[{"id":"T9668","span":{"begin":1171,"end":1296},"obj":"Sentence"},{"id":"T9667","span":{"begin":1045,"end":1170},"obj":"Sentence"},{"id":"T9666","span":{"begin":820,"end":1044},"obj":"Sentence"},{"id":"T9665","span":{"begin":726,"end":819},"obj":"Sentence"},{"id":"T9664","span":{"begin":545,"end":725},"obj":"Sentence"},{"id":"T9663","span":{"begin":324,"end":544},"obj":"Sentence"},{"id":"T9662","span":{"begin":161,"end":323},"obj":"Sentence"},{"id":"T9661","span":{"begin":0,"end":160},"obj":"Sentence"},{"id":"T118","span":{"begin":0,"end":160},"obj":"Sentence"},{"id":"T119","span":{"begin":161,"end":323},"obj":"Sentence"},{"id":"T120","span":{"begin":324,"end":544},"obj":"Sentence"},{"id":"T121","span":{"begin":545,"end":725},"obj":"Sentence"},{"id":"T122","span":{"begin":726,"end":819},"obj":"Sentence"},{"id":"T123","span":{"begin":820,"end":1044},"obj":"Sentence"},{"id":"T124","span":{"begin":1045,"end":1170},"obj":"Sentence"},{"id":"T125","span":{"begin":1171,"end":1296},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"simple1","denotations":[{"id":"T10796","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T10795","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T10794","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T10793","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T10792","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T10791","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T10790","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T10789","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T10788","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T10787","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T10786","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T10785","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T10784","span":{"begin":39,"end":42},"obj":"Protein"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T12275","span":{"begin":977,"end":986},"obj":"Negative_regulation"},{"id":"T12274","span":{"begin":991,"end":1004},"obj":"Transcription"},{"id":"T12273","span":{"begin":745,"end":751},"obj":"Regulation"},{"id":"T12272","span":{"begin":587,"end":594},"obj":"Positive_regulation"},{"id":"T12271","span":{"begin":555,"end":563},"obj":"Positive_regulation"},{"id":"T12270","span":{"begin":404,"end":413},"obj":"Regulation"},{"id":"T12269","span":{"begin":223,"end":234},"obj":"Binding"},{"id":"T12242","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T12241","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T12240","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T12239","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T12238","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T12237","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T12236","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T12235","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T12234","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T12233","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T12232","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T12231","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T12230","span":{"begin":39,"end":42},"obj":"Protein"}],"relations":[{"id":"R8243","pred":"themeOf","subj":"T12274","obj":"T12275"},{"id":"R8264","pred":"themeOf","subj":"T12231","obj":"T12269"},{"id":"R8265","pred":"themeOf","subj":"T12232","obj":"T12270"},{"id":"R8266","pred":"themeOf","subj":"T12234","obj":"T12271"},{"id":"R8267","pred":"themeOf","subj":"T12235","obj":"T12272"},{"id":"R8268","pred":"themeOf","subj":"T12239","obj":"T12273"},{"id":"R8269","pred":"themeOf","subj":"T12241","obj":"T12274"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"BioNLP16_Messiy","denotations":[{"id":"T11833","span":{"begin":977,"end":986},"obj":"Negative_regulation"},{"id":"T11805","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T11804","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T11803","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T11802","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T11801","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T11800","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T11799","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T11798","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T11797","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T11796","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T11795","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T11794","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T11793","span":{"begin":39,"end":42},"obj":"Protein"},{"id":"T11832","span":{"begin":991,"end":1004},"obj":"Transcription"},{"id":"T11831","span":{"begin":555,"end":563},"obj":"Positive_regulation"},{"id":"T11830","span":{"begin":587,"end":594},"obj":"Positive_regulation"},{"id":"T11829","span":{"begin":404,"end":413},"obj":"Regulation"},{"id":"T11828","span":{"begin":223,"end":234},"obj":"Binding"}],"relations":[{"id":"R8074","pred":"themeOf","subj":"T11794","obj":"T11828"},{"id":"R8076","pred":"themeOf","subj":"T11795","obj":"T11829"},{"id":"R8078","pred":"themeOf","subj":"T11797","obj":"T11831"},{"id":"R8079","pred":"themeOf","subj":"T11798","obj":"T11830"},{"id":"R8082","pred":"themeOf","subj":"T11804","obj":"T11832"},{"id":"R8101","pred":"themeOf","subj":"T11832","obj":"T11833"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"bionlp-st-ge-2016-test-ihmc","denotations":[{"id":"T12412","span":{"begin":215,"end":252},"obj":"Binding"},{"id":"T12411","span":{"begin":977,"end":1004},"obj":"Negative_regulation"},{"id":"T12406","span":{"begin":966,"end":1004},"obj":"Transcription"},{"id":"T12402","span":{"begin":939,"end":951},"obj":"Entity"},{"id":"T12400","span":{"begin":722,"end":724},"obj":"Protein"},{"id":"T12398","span":{"begin":1264,"end":1266},"obj":"Protein"},{"id":"T12397","span":{"begin":791,"end":793},"obj":"Protein"},{"id":"T12394","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T12393","span":{"begin":376,"end":382},"obj":"Protein"},{"id":"T12385","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T12373","span":{"begin":652,"end":654},"obj":"Protein"},{"id":"T12354","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T12353","span":{"begin":421,"end":437},"obj":"Protein"},{"id":"T12349","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T12348","span":{"begin":39,"end":42},"obj":"Protein"},{"id":"T12327","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T12321","span":{"begin":315,"end":322},"obj":"Protein"},{"id":"T12320","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T12319","span":{"begin":906,"end":922},"obj":"Entity"},{"id":"T12315","span":{"begin":615,"end":654},"obj":"Protein"},{"id":"T12298","span":{"begin":256,"end":263},"obj":"Protein"},{"id":"T12292","span":{"begin":583,"end":594},"obj":"Protein"},{"id":"T12291","span":{"begin":516,"end":519},"obj":"Entity"},{"id":"T12290","span":{"begin":273,"end":292},"obj":"Entity"},{"id":"T12288","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T12283","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T12282","span":{"begin":608,"end":611},"obj":"Protein"}],"relations":[{"id":"R8261","pred":"themeOf","subj":"T12283","obj":"T12406"},{"id":"R8287","pred":"partOf","subj":"T12402","obj":"T12385"},{"id":"R8290","pred":"themeOf","subj":"T12406","obj":"T12411"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T12010","span":{"begin":1223,"end":1231},"obj":"Protein"},{"id":"T12009","span":{"begin":939,"end":951},"obj":"Protein"},{"id":"T12008","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T12007","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T12006","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T12005","span":{"begin":260,"end":269},"obj":"Protein"},{"id":"T12004","span":{"begin":33,"end":48},"obj":"Protein"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}

{"project":"test3","denotations":[{"id":"T9631","span":{"begin":1223,"end":1226},"obj":"Protein"},{"id":"T9630","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T9629","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T9628","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T9627","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T9626","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T9625","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T9624","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T9623","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T9622","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T9621","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T9620","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T9619","span":{"begin":39,"end":42},"obj":"Protein"},{"id":"T9557","span":{"begin":987,"end":990},"obj":"Protein"},{"id":"T9556","span":{"begin":939,"end":942},"obj":"Protein"},{"id":"T9555","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T9554","span":{"begin":678,"end":681},"obj":"Protein"},{"id":"T9553","span":{"begin":640,"end":648},"obj":"Protein"},{"id":"T9552","span":{"begin":608,"end":611},"obj":"Protein"},{"id":"T9551","span":{"begin":583,"end":586},"obj":"Protein"},{"id":"T9550","span":{"begin":548,"end":551},"obj":"Protein"},{"id":"T9549","span":{"begin":461,"end":464},"obj":"Protein"},{"id":"T9548","span":{"begin":414,"end":417},"obj":"Protein"},{"id":"T9547","span":{"begin":260,"end":263},"obj":"Protein"},{"id":"T9546","span":{"begin":39,"end":42},"obj":"Protein"},{"id":"T9558","span":{"begin":1223,"end":1226},"obj":"Protein"}],"text":"Importantly, several SNPs in the human A20 locus have been associated with increased susceptibility to development of autoimmune pathologies (reviewed in [52]). Several genome-wide association studies also revealed a clear association between mutations in the A20 locus in the 6q23 chromosome and susceptibility to RA [52]. Although the identified variants are not located in a gene, they are thought to influence A20 as its nearest gene (~150 kb downstream of A20), probably by the presence of potential regulatory DNA elements in this region. As A20 is required for termination of TNF-induced signals, and TNF is the primary inflammatory cytokine in RA, these findings reveal A20 as a candidate susceptibility locus for RA. How these variants affect normal A20 activity and how they cause RA, however, remain unclear. Recently, Elsby and colleagues functionally evaluated in vitro the regulatory ability of RA-associated SNP variants on A20 promoter activity, and could show repressed A20 transcription for some of the SNPs investigated [53]. It will be of interest to identify the actual causal variants and to elucidate the functional consequences of these variants. In this context, knockin mice for the corresponding A20 SNPs, combined with mouse models for RA, will be very valuable tools."}