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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
13
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pubmed:dateCreated |
2006-12-6
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pubmed:abstractText |
The t(5;14)(q35;q32) chromosomal translocation is specifically observed in up to 20% of childhood T-cell acute lymphoblastic leukemia (T-ALL). It affects the BCL11B/CTIP2 locus on chromosome 14 and the RANBP17-TLX3/HOX11L2 region on chromosome 5. It leads to ectopic activation of TLX3/HOX11L2. To investigate the reasons of the association between t(5;14) and T-ALL, we isolated the translocation breakpoints in 8 t(5;14) patients. Sequence analyses did not involve recombinase activity in the genesis of the translocation. We used DNAse1 hypersensitive experiments to locate transcriptional regulatory elements downstream of BCL11B. By transient transfection experiments, 2 of the 6 regions demonstrated cis-activation properties in T cells and were also effective on the TLX3 promoter. Our data indicate that the basis of the specific association between t(5;14) and T-ALL lies on the juxtaposition of TLX3 to long-range cis-activating regions active during T-cell differentiation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/BCL11B protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Fusion,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/TLX3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0006-4971
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pubmed:author |
pubmed-author:Andre-SchmutzIsabelleI,
pubmed-author:BalleriniPaolaP,
pubmed-author:BergerRolandR,
pubmed-author:BernardOlivier AOA,
pubmed-author:Della-ValleVéroniqueV,
pubmed-author:Lafage-PochitaloffMarinaM,
pubmed-author:LemercierClaudieC,
pubmed-author:LessardMichelM,
pubmed-author:MugneretFrancineF,
pubmed-author:Penard-LacroniqueVirginieV,
pubmed-author:Radford-WeissIsabelleI,
pubmed-author:RomanaSerge PSP,
pubmed-author:SuXin-YingXY
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4198-201
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16926283-Cell Differentiation,
pubmed-meshheading:16926283-Chromosomes, Human, Pair 14,
pubmed-meshheading:16926283-Chromosomes, Human, Pair 5,
pubmed-meshheading:16926283-DNA-Binding Proteins,
pubmed-meshheading:16926283-Homeodomain Proteins,
pubmed-meshheading:16926283-Humans,
pubmed-meshheading:16926283-Jurkat Cells,
pubmed-meshheading:16926283-Leukemia-Lymphoma, Adult T-Cell,
pubmed-meshheading:16926283-Oncogene Proteins,
pubmed-meshheading:16926283-Oncogene Proteins, Fusion,
pubmed-meshheading:16926283-Promoter Regions, Genetic,
pubmed-meshheading:16926283-Repressor Proteins,
pubmed-meshheading:16926283-T-Lymphocytes,
pubmed-meshheading:16926283-Transcription, Genetic,
pubmed-meshheading:16926283-Translocation, Genetic,
pubmed-meshheading:16926283-Tumor Suppressor Proteins
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pubmed:year |
2006
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pubmed:articleTitle |
HOX11L2/TLX3 is transcriptionally activated through T-cell regulatory elements downstream of BCL11B as a result of the t(5;14)(q35;q32).
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale (INSERM), E0210, Paris, France.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, Non-U.S. Gov't
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