PMC:3342329 / 195-1688
Annnotations
test3
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testone
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BioNLP16_Messiy
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BioNLP16_DUT
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evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
bionlp-st-ge-2016-test-proteins
{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T186","span":{"begin":1486,"end":1492},"obj":"Protein"},{"id":"T185","span":{"begin":1382,"end":1386},"obj":"Protein"},{"id":"T184","span":{"begin":1331,"end":1335},"obj":"Protein"},{"id":"T183","span":{"begin":1298,"end":1302},"obj":"Protein"},{"id":"T182","span":{"begin":1138,"end":1142},"obj":"Protein"},{"id":"T181","span":{"begin":1100,"end":1104},"obj":"Protein"},{"id":"T180","span":{"begin":998,"end":1004},"obj":"Protein"},{"id":"T179","span":{"begin":942,"end":946},"obj":"Protein"},{"id":"T178","span":{"begin":893,"end":899},"obj":"Protein"},{"id":"T177","span":{"begin":709,"end":713},"obj":"Protein"},{"id":"T176","span":{"begin":664,"end":668},"obj":"Protein"},{"id":"T175","span":{"begin":557,"end":560},"obj":"Protein"},{"id":"T174","span":{"begin":549,"end":552},"obj":"Protein"},{"id":"T173","span":{"begin":291,"end":295},"obj":"Protein"},{"id":"T172","span":{"begin":190,"end":194},"obj":"Protein"},{"id":"T171","span":{"begin":175,"end":179},"obj":"Protein"},{"id":"T170","span":{"begin":146,"end":150},"obj":"Protein"},{"id":"T169","span":{"begin":131,"end":135},"obj":"Protein"},{"id":"T168","span":{"begin":60,"end":64},"obj":"Protein"},{"id":"T167","span":{"begin":29,"end":58},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
bionlp-st-ge-2016-uniprot
{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T554","span":{"begin":1178,"end":1181},"obj":"http://www.uniprot.org/uniprot/P10966"},{"id":"T553","span":{"begin":1178,"end":1181},"obj":"http://www.uniprot.org/uniprot/P01732"},{"id":"T552","span":{"begin":893,"end":899},"obj":"http://www.uniprot.org/uniprot/Q13490"},{"id":"T551","span":{"begin":782,"end":791},"obj":"http://www.uniprot.org/uniprot/P42574"},{"id":"T550","span":{"begin":557,"end":560},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T549","span":{"begin":557,"end":560},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T548","span":{"begin":549,"end":552},"obj":"http://www.uniprot.org/uniprot/P19838"},{"id":"T547","span":{"begin":1382,"end":1386},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T546","span":{"begin":1331,"end":1335},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T545","span":{"begin":1298,"end":1302},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T544","span":{"begin":1138,"end":1142},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T543","span":{"begin":1100,"end":1104},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T542","span":{"begin":942,"end":946},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T541","span":{"begin":709,"end":713},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T540","span":{"begin":664,"end":668},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T539","span":{"begin":291,"end":295},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T538","span":{"begin":190,"end":194},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T537","span":{"begin":175,"end":179},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T536","span":{"begin":146,"end":150},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T535","span":{"begin":131,"end":135},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T534","span":{"begin":60,"end":64},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T533","span":{"begin":1486,"end":1492},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T532","span":{"begin":998,"end":1004},"obj":"http://www.uniprot.org/uniprot/P18510"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
UBERON-AE
{"project":"UBERON-AE","denotations":[{"id":"T119","span":{"begin":1281,"end":1287},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"T118","span":{"begin":1090,"end":1096},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"T117","span":{"begin":1288,"end":1294},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T116","span":{"begin":1079,"end":1085},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T115","span":{"begin":931,"end":938},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T114","span":{"begin":698,"end":705},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T113","span":{"begin":653,"end":660},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
GO-BP
{"project":"GO-BP","denotations":[{"id":"T209","span":{"begin":1420,"end":1425},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T208","span":{"begin":1415,"end":1425},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T207","span":{"begin":604,"end":626},"obj":"http://purl.obolibrary.org/obo/GO_0007252"},{"id":"T206","span":{"begin":604,"end":619},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T205","span":{"begin":590,"end":626},"obj":"http://purl.obolibrary.org/obo/GO_1903720"},{"id":"T204","span":{"begin":590,"end":619},"obj":"http://purl.obolibrary.org/obo/GO_0042326"},{"id":"T203","span":{"begin":483,"end":508},"obj":"http://purl.obolibrary.org/obo/GO_0039568"},{"id":"T202","span":{"begin":483,"end":508},"obj":"http://purl.obolibrary.org/obo/GO_1904743"},{"id":"T201","span":{"begin":483,"end":508},"obj":"http://purl.obolibrary.org/obo/GO_0043392"},{"id":"T200","span":{"begin":442,"end":451},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T199","span":{"begin":1405,"end":1425},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T198","span":{"begin":442,"end":451},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T197","span":{"begin":429,"end":440},"obj":"http://purl.obolibrary.org/obo/GO_0016049"},{"id":"T196","span":{"begin":399,"end":409},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T195","span":{"begin":371,"end":409},"obj":"http://purl.obolibrary.org/obo/GO_0051090"},{"id":"T194","span":{"begin":371,"end":409},"obj":"http://purl.obolibrary.org/obo/GO_1901483"},{"id":"T193","span":{"begin":371,"end":384},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T192","span":{"begin":325,"end":344},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T191","span":{"begin":1014,"end":1020},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T190","span":{"begin":463,"end":469},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T189","span":{"begin":434,"end":440},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T188","span":{"begin":121,"end":127},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T187","span":{"begin":87,"end":98},"obj":"http://purl.obolibrary.org/obo/GO_0032502"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
GO-MF
{"project":"GO-MF","denotations":[{"id":"T214","span":{"begin":497,"end":508},"obj":"http://purl.obolibrary.org/obo/GO_0003677"},{"id":"T215","span":{"begin":501,"end":508},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
GO-CC
{"project":"GO-CC","denotations":[{"id":"T210","span":{"begin":429,"end":433},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T211","span":{"begin":1195,"end":1199},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T212","span":{"begin":1415,"end":1419},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T213","span":{"begin":570,"end":577},"obj":"http://purl.obolibrary.org/obo/GO_0005634"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
sentences
{"project":"sentences","denotations":[{"id":"T128","span":{"begin":1345,"end":1493},"obj":"Sentence"},{"id":"T127","span":{"begin":1152,"end":1344},"obj":"Sentence"},{"id":"T126","span":{"begin":956,"end":1151},"obj":"Sentence"},{"id":"T125","span":{"begin":723,"end":955},"obj":"Sentence"},{"id":"T124","span":{"begin":471,"end":722},"obj":"Sentence"},{"id":"T123","span":{"begin":305,"end":470},"obj":"Sentence"},{"id":"T122","span":{"begin":190,"end":304},"obj":"Sentence"},{"id":"T121","span":{"begin":0,"end":189},"obj":"Sentence"},{"id":"T4","span":{"begin":0,"end":189},"obj":"Sentence"},{"id":"T5","span":{"begin":190,"end":304},"obj":"Sentence"},{"id":"T6","span":{"begin":305,"end":470},"obj":"Sentence"},{"id":"T7","span":{"begin":471,"end":722},"obj":"Sentence"},{"id":"T8","span":{"begin":723,"end":955},"obj":"Sentence"},{"id":"T9","span":{"begin":956,"end":1151},"obj":"Sentence"},{"id":"T10","span":{"begin":1152,"end":1344},"obj":"Sentence"},{"id":"T11","span":{"begin":1345,"end":1493},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
simple1
{"project":"simple1","denotations":[{"id":"T259","span":{"begin":1486,"end":1492},"obj":"Protein"},{"id":"T258","span":{"begin":1382,"end":1386},"obj":"Protein"},{"id":"T257","span":{"begin":1331,"end":1335},"obj":"Protein"},{"id":"T256","span":{"begin":1298,"end":1302},"obj":"Protein"},{"id":"T255","span":{"begin":1138,"end":1142},"obj":"Protein"},{"id":"T254","span":{"begin":1100,"end":1104},"obj":"Protein"},{"id":"T253","span":{"begin":998,"end":1004},"obj":"Protein"},{"id":"T252","span":{"begin":942,"end":946},"obj":"Protein"},{"id":"T251","span":{"begin":893,"end":899},"obj":"Protein"},{"id":"T250","span":{"begin":709,"end":713},"obj":"Protein"},{"id":"T249","span":{"begin":664,"end":668},"obj":"Protein"},{"id":"T248","span":{"begin":557,"end":560},"obj":"Protein"},{"id":"T247","span":{"begin":549,"end":552},"obj":"Protein"},{"id":"T246","span":{"begin":291,"end":295},"obj":"Protein"},{"id":"T245","span":{"begin":190,"end":194},"obj":"Protein"},{"id":"T244","span":{"begin":175,"end":179},"obj":"Protein"},{"id":"T243","span":{"begin":146,"end":150},"obj":"Protein"},{"id":"T242","span":{"begin":131,"end":135},"obj":"Protein"},{"id":"T241","span":{"begin":60,"end":64},"obj":"Protein"},{"id":"T240","span":{"begin":29,"end":58},"obj":"Protein"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
DLUT931
{"project":"DLUT931","denotations":[{"id":"T587","span":{"begin":1446,"end":1456},"obj":"Negative_regulation"},{"id":"T586","span":{"begin":1470,"end":1482},"obj":"Positive_regulation"},{"id":"T585","span":{"begin":1387,"end":1397},"obj":"Negative_regulation"},{"id":"T584","span":{"begin":1061,"end":1069},"obj":"Positive_regulation"},{"id":"T583","span":{"begin":905,"end":914},"obj":"Negative_regulation"},{"id":"T582","span":{"begin":859,"end":869},"obj":"Gene_expression"},{"id":"T581","span":{"begin":590,"end":600},"obj":"Negative_regulation"},{"id":"T580","span":{"begin":532,"end":545},"obj":"Localization"},{"id":"T579","span":{"begin":136,"end":144},"obj":"Negative_regulation"},{"id":"T578","span":{"begin":66,"end":76},"obj":"Gene_expression"},{"id":"T576","span":{"begin":1486,"end":1492},"obj":"Protein"},{"id":"T575","span":{"begin":1382,"end":1386},"obj":"Protein"},{"id":"T574","span":{"begin":1331,"end":1335},"obj":"Protein"},{"id":"T573","span":{"begin":1298,"end":1302},"obj":"Protein"},{"id":"T572","span":{"begin":1138,"end":1142},"obj":"Protein"},{"id":"T571","span":{"begin":1100,"end":1104},"obj":"Protein"},{"id":"T570","span":{"begin":998,"end":1004},"obj":"Protein"},{"id":"T569","span":{"begin":942,"end":946},"obj":"Protein"},{"id":"T568","span":{"begin":893,"end":899},"obj":"Protein"},{"id":"T567","span":{"begin":709,"end":713},"obj":"Protein"},{"id":"T566","span":{"begin":664,"end":668},"obj":"Protein"},{"id":"T565","span":{"begin":557,"end":560},"obj":"Protein"},{"id":"T564","span":{"begin":549,"end":552},"obj":"Protein"},{"id":"T563","span":{"begin":291,"end":295},"obj":"Protein"},{"id":"T562","span":{"begin":190,"end":194},"obj":"Protein"},{"id":"T561","span":{"begin":175,"end":179},"obj":"Protein"},{"id":"T560","span":{"begin":146,"end":150},"obj":"Protein"},{"id":"T559","span":{"begin":131,"end":135},"obj":"Protein"},{"id":"T558","span":{"begin":60,"end":64},"obj":"Protein"},{"id":"T557","span":{"begin":29,"end":58},"obj":"Protein"}],"relations":[{"id":"R314","pred":"themeOf","subj":"T557","obj":"T578"},{"id":"R315","pred":"themeOf","subj":"T558","obj":"T578"},{"id":"R316","pred":"themeOf","subj":"T559","obj":"T579"},{"id":"R317","pred":"themeOf","subj":"T560","obj":"T579"},{"id":"R318","pred":"themeOf","subj":"T564","obj":"T580"},{"id":"R319","pred":"themeOf","subj":"T565","obj":"T580"},{"id":"R320","pred":"themeOf","subj":"T568","obj":"T582"},{"id":"R321","pred":"themeOf","subj":"T570","obj":"T584"},{"id":"R322","pred":"themeOf","subj":"T575","obj":"T585"},{"id":"R323","pred":"themeOf","subj":"T576","obj":"T586"},{"id":"R324","pred":"themeOf","subj":"T580","obj":"T581"},{"id":"R325","pred":"themeOf","subj":"T580","obj":"T581"},{"id":"R326","pred":"themeOf","subj":"T582","obj":"T583"},{"id":"R327","pred":"causeOf","subj":"T585","obj":"T586"},{"id":"R328","pred":"causeOf","subj":"T585","obj":"T587"},{"id":"R329","pred":"themeOf","subj":"T586","obj":"T587"}],"text":"To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
bionlp-st-ge-2016-test-ihmc
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evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5−/−) mice and wild type (CCR5+/+) mice. CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. Moreover, infiltration of CD8+ cytotoxic T cell and CD57+ natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5−/− mice compared to that of CCR5+/+ mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra."}
bionlp-st-ge-2016-test-tees
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CCR5−/− mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5+/+ mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5−/− mice compared to melanoma tissues of CCR5+/+ mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5−/− mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5−/− mice compared to the level in CCR5+/+ mice. 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