PubMed:10482545 JSON TXT

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PMID_GLOBAL

{"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":42,"end":57},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":153,"end":168},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005525"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005525"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005801"}],"text":"Induction of Bcl-x(L) expression by human T-cell leukemia virus type 1 Tax through NF-kappaB in apoptosis-resistant T-cell transfectants with Tax.\nHuman T-cell leukemia virus type 1 (HTLV-1) Tax is thought to play a pivotal role in immortalization of T cells. We have recently shown that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by interleukin-2 (IL-2) deprivation and converted its growth from being IL-2 dependent to being IL-2 independent. In this study, we demonstrate that constitutive expression of bcl-xl but not bcl-2, bcl-xs, bak, bad, or bax was associated with apoptosis resistance after IL-2 deprivation in CTLL-2 cells that expressed Tax. Transient-transfection assays showed that bcl-x promoter was transactivated by wild-type Tax. Similar effects were observed in mutant Tax retaining transactivating ability through NF-kappaB. Deletion or substitution of a putative NF-kappaB binding site identified in the bcl-x promoter significantly decreased Tax-induced transactivation. This NF-kappaB-like element was able to form a complex with NF-kappaB family proteins in vitro. Furthermore, Tax-induced transactivation of the bcl-x promoter was also diminished by the mutant IkappaBalpha, which specifically inhibits NF-kappaB activity. Our findings suggest that constitutive expression of Bcl-x(L) induced by Tax through the NF-kappaB pathway contributes to the inhibition of apoptosis in CTLL-2 cells after IL-2 deprivation."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":160,"end":168},"obj":"HP_0001909"}],"text":"Induction of Bcl-x(L) expression by human T-cell leukemia virus type 1 Tax through NF-kappaB in apoptosis-resistant T-cell transfectants with Tax.\nHuman T-cell leukemia virus type 1 (HTLV-1) Tax is thought to play a pivotal role in immortalization of T cells. We have recently shown that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by interleukin-2 (IL-2) deprivation and converted its growth from being IL-2 dependent to being IL-2 independent. In this study, we demonstrate that constitutive expression of bcl-xl but not bcl-2, bcl-xs, bak, bad, or bax was associated with apoptosis resistance after IL-2 deprivation in CTLL-2 cells that expressed Tax. Transient-transfection assays showed that bcl-x promoter was transactivated by wild-type Tax. Similar effects were observed in mutant Tax retaining transactivating ability through NF-kappaB. Deletion or substitution of a putative NF-kappaB binding site identified in the bcl-x promoter significantly decreased Tax-induced transactivation. This NF-kappaB-like element was able to form a complex with NF-kappaB family proteins in vitro. Furthermore, Tax-induced transactivation of the bcl-x promoter was also diminished by the mutant IkappaBalpha, which specifically inhibits NF-kappaB activity. Our findings suggest that constitutive expression of Bcl-x(L) induced by Tax through the NF-kappaB pathway contributes to the inhibition of apoptosis in CTLL-2 cells after IL-2 deprivation."}

jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":13,"end":21},"obj":"protein"},{"id":"T2","span":{"begin":36,"end":74},"obj":"protein"},{"id":"T3","span":{"begin":83,"end":92},"obj":"protein"},{"id":"T4","span":{"begin":96,"end":136},"obj":"cell_line"},{"id":"T5","span":{"begin":142,"end":145},"obj":"protein"},{"id":"T6","span":{"begin":191,"end":194},"obj":"protein"},{"id":"T7","span":{"begin":251,"end":258},"obj":"cell_type"},{"id":"T8","span":{"begin":306,"end":309},"obj":"protein"},{"id":"T9","span":{"begin":324,"end":348},"obj":"cell_line"},{"id":"T10","span":{"begin":378,"end":391},"obj":"protein"},{"id":"T11","span":{"begin":393,"end":397},"obj":"protein"},{"id":"T12","span":{"begin":447,"end":451},"obj":"protein"},{"id":"T13","span":{"begin":471,"end":475},"obj":"protein"},{"id":"T14","span":{"begin":551,"end":557},"obj":"protein"},{"id":"T15","span":{"begin":566,"end":571},"obj":"protein"},{"id":"T16","span":{"begin":573,"end":579},"obj":"protein"},{"id":"T17","span":{"begin":581,"end":584},"obj":"protein"},{"id":"T18","span":{"begin":586,"end":589},"obj":"protein"},{"id":"T19","span":{"begin":594,"end":597},"obj":"protein"},{"id":"T20","span":{"begin":645,"end":649},"obj":"protein"},{"id":"T21","span":{"begin":665,"end":677},"obj":"cell_line"},{"id":"T22","span":{"begin":693,"end":696},"obj":"protein"},{"id":"T23","span":{"begin":740,"end":754},"obj":"DNA"},{"id":"T24","span":{"begin":777,"end":790},"obj":"protein"},{"id":"T25","span":{"begin":832,"end":835},"obj":"protein"},{"id":"T26","span":{"begin":878,"end":887},"obj":"protein"},{"id":"T27","span":{"begin":919,"end":950},"obj":"protein"},{"id":"T28","span":{"begin":969,"end":983},"obj":"DNA"},{"id":"T29","span":{"begin":1008,"end":1011},"obj":"protein"},{"id":"T30","span":{"begin":1042,"end":1064},"obj":"DNA"},{"id":"T31","span":{"begin":1097,"end":1122},"obj":"protein"},{"id":"T32","span":{"begin":1146,"end":1149},"obj":"protein"},{"id":"T33","span":{"begin":1181,"end":1195},"obj":"DNA"},{"id":"T34","span":{"begin":1223,"end":1242},"obj":"protein"},{"id":"T35","span":{"begin":1272,"end":1281},"obj":"protein"},{"id":"T36","span":{"begin":1345,"end":1353},"obj":"protein"},{"id":"T37","span":{"begin":1365,"end":1368},"obj":"protein"},{"id":"T38","span":{"begin":1381,"end":1390},"obj":"protein"},{"id":"T39","span":{"begin":1445,"end":1457},"obj":"cell_line"},{"id":"T40","span":{"begin":1464,"end":1468},"obj":"protein"}],"text":"Induction of Bcl-x(L) expression by human T-cell leukemia virus type 1 Tax through NF-kappaB in apoptosis-resistant T-cell transfectants with Tax.\nHuman T-cell leukemia virus type 1 (HTLV-1) Tax is thought to play a pivotal role in immortalization of T cells. We have recently shown that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by interleukin-2 (IL-2) deprivation and converted its growth from being IL-2 dependent to being IL-2 independent. In this study, we demonstrate that constitutive expression of bcl-xl but not bcl-2, bcl-xs, bak, bad, or bax was associated with apoptosis resistance after IL-2 deprivation in CTLL-2 cells that expressed Tax. Transient-transfection assays showed that bcl-x promoter was transactivated by wild-type Tax. Similar effects were observed in mutant Tax retaining transactivating ability through NF-kappaB. Deletion or substitution of a putative NF-kappaB binding site identified in the bcl-x promoter significantly decreased Tax-induced transactivation. This NF-kappaB-like element was able to form a complex with NF-kappaB family proteins in vitro. Furthermore, Tax-induced transactivation of the bcl-x promoter was also diminished by the mutant IkappaBalpha, which specifically inhibits NF-kappaB activity. Our findings suggest that constitutive expression of Bcl-x(L) induced by Tax through the NF-kappaB pathway contributes to the inhibition of apoptosis in CTLL-2 cells after IL-2 deprivation."}

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":146},"obj":"Sentence"},{"id":"S2","span":{"begin":147,"end":259},"obj":"Sentence"},{"id":"S3","span":{"begin":260,"end":488},"obj":"Sentence"},{"id":"S4","span":{"begin":489,"end":697},"obj":"Sentence"},{"id":"S5","span":{"begin":698,"end":791},"obj":"Sentence"},{"id":"S6","span":{"begin":792,"end":888},"obj":"Sentence"},{"id":"S7","span":{"begin":889,"end":1036},"obj":"Sentence"},{"id":"S8","span":{"begin":1037,"end":1132},"obj":"Sentence"},{"id":"S9","span":{"begin":1133,"end":1291},"obj":"Sentence"},{"id":"S10","span":{"begin":1292,"end":1481},"obj":"Sentence"}],"text":"Induction of Bcl-x(L) expression by human T-cell leukemia virus type 1 Tax through NF-kappaB in apoptosis-resistant T-cell transfectants with Tax.\nHuman T-cell leukemia virus type 1 (HTLV-1) Tax is thought to play a pivotal role in immortalization of T cells. We have recently shown that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by interleukin-2 (IL-2) deprivation and converted its growth from being IL-2 dependent to being IL-2 independent. In this study, we demonstrate that constitutive expression of bcl-xl but not bcl-2, bcl-xs, bak, bad, or bax was associated with apoptosis resistance after IL-2 deprivation in CTLL-2 cells that expressed Tax. Transient-transfection assays showed that bcl-x promoter was transactivated by wild-type Tax. Similar effects were observed in mutant Tax retaining transactivating ability through NF-kappaB. Deletion or substitution of a putative NF-kappaB binding site identified in the bcl-x promoter significantly decreased Tax-induced transactivation. This NF-kappaB-like element was able to form a complex with NF-kappaB family proteins in vitro. Furthermore, Tax-induced transactivation of the bcl-x promoter was also diminished by the mutant IkappaBalpha, which specifically inhibits NF-kappaB activity. Our findings suggest that constitutive expression of Bcl-x(L) induced by Tax through the NF-kappaB pathway contributes to the inhibition of apoptosis in CTLL-2 cells after IL-2 deprivation."}

genia-medco-coref

GENIAcorpus