rdf:type |
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lifeskim:mentions |
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pubmed:issue |
40
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pubmed:dateCreated |
2010-9-27
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pubmed:abstractText |
The transcription factor C/EBP? is more potent than C/EBP? in inducing granulocitic differentiation and inhibiting BCR/ABL-expressing cells. We took a "domain swapping" approach to assess biological effects, modulation of gene expression, and binding to C/EBP?-regulated promoters by wild-type and chimeric C/EBP?/C/EBP? proteins. Wild-type and N-C/EBP?+ C/EBP?-DBD induced transcription of the granulocyte-colony stimulating factor receptor (G-CSFR) gene, promoted differentiation, and suppressed proliferation of K562 cells vigorously; instead, wild-type C/EBP? and N-C/EBP?+C/EBP?-DBD had modest effects, although they bound the G-CSFR promoter like wild-type C/EBP? and N-C/EBP?+C/EBP?-DBD. Chimeric proteins consisting of the TAD of VP16 and the DBD of C/EBP? or C/EBP? inhibited proliferation and induced differentiation of K562 cells as effectively as wild-type C/EBP?. Gene expression profiles induced by C/EBP? resembled those modulated by N-C/EBP?+C/EBP?-DBD, whereas C/EBP? induced a pattern similar to that of N-C/EBP?+C/EBP?-DBD. C/EBP? activation induced changes in the expression of more cell cycle- and apoptosis-related genes than the other proteins and enhanced Imatinib-induced apoptosis of K562 cells. Expression of FOXO3a, a novel C/EBP?-regulated gene, was required for apoptosis but not for differentiation induction or proliferation inhibition of K562 cells.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Protein-beta,
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/CEBPA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CEBPB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/FOXO3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
|
pubmed:issn |
1083-351X
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pubmed:author |
pubmed-author:CalabrettaBrunoB,
pubmed-author:CattelaniSaraS,
pubmed-author:CorradiniFrancescaF,
pubmed-author:Ferrari-AmorottiGiovannaG,
pubmed-author:FragliassoValentinaV,
pubmed-author:GuerzoniClaraC,
pubmed-author:LamEric W-FEW,
pubmed-author:ManzottiGloriaG,
pubmed-author:MarianiSamanta AntonellaSA,
pubmed-author:MartinezRobert VRV,
pubmed-author:NoviChiaraC,
pubmed-author:PecorariLuisaL,
pubmed-author:SolieraAngela RacheleAR,
pubmed-author:ZhangYingY
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
285
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
30837-50
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pubmed:dateRevised |
2011-10-3
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pubmed:meshHeading |
pubmed-meshheading:20659895-Apoptosis,
pubmed-meshheading:20659895-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:20659895-CCAAT-Enhancer-Binding Proteins,
pubmed-meshheading:20659895-Cell Cycle,
pubmed-meshheading:20659895-Cell Differentiation,
pubmed-meshheading:20659895-Forkhead Transcription Factors,
pubmed-meshheading:20659895-Gene Expression Regulation,
pubmed-meshheading:20659895-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:20659895-Humans,
pubmed-meshheading:20659895-K562 Cells,
pubmed-meshheading:20659895-Promoter Regions, Genetic,
pubmed-meshheading:20659895-Protein Structure, Tertiary,
pubmed-meshheading:20659895-Recombinant Fusion Proteins,
pubmed-meshheading:20659895-Transcription, Genetic
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pubmed:year |
2010
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pubmed:articleTitle |
The biological effects of C/EBPalpha in K562 cells depend on the potency of the N-terminal regulatory region, not on specificity of the DNA binding domain.
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pubmed:affiliation |
Department of Biological Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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