rdf:type |
|
lifeskim:mentions |
umls-concept:C0017337,
umls-concept:C0020792,
umls-concept:C0028589,
umls-concept:C0040649,
umls-concept:C0086222,
umls-concept:C0086418,
umls-concept:C0087048,
umls-concept:C0205214,
umls-concept:C0205245,
umls-concept:C0330390,
umls-concept:C0524891,
umls-concept:C1564097,
umls-concept:C1705733,
umls-concept:C1880022
|
pubmed:issue |
10
|
pubmed:dateCreated |
1990-10-18
|
pubmed:databankReference |
|
pubmed:abstractText |
A transcriptional enhancer has been mapped to a region 5.5 kilobases 3' of the C beta 2 gene in the human T-cell receptor (TCR) beta-chain locus. Transient transfections allowed localization of enhancer activity to a 480-base-pair HincII-XbaI restriction enzyme fragment. The TCR beta enhancer was active on both the minimal simian virus 40 promoter and a TCR beta variable gene promoter in both TCR alpha/beta + and TCR gamma/delta + T cells. It displayed significantly less activity in Epstein-Barr virus-transformed B cells and K562 chronic myelogenous leukemia cells and no activity in HeLa fibroblasts. DNA sequence analysis revealed that the enhancer contains a consensus immunoglobulin kappa E2 motif, as well as an AP-1-binding site and a cyclic AMP response element. DNase I footprint analyses using Jurkat T-cell nuclear extracts allowed the identification of five nuclear protein-binding sites, T beta 1 to T beta 5, within the enhancer element. Deletion and in vitro mutagenesis studies demonstrated that the T beta 2- and T beta 3- and T beta 4-binding sites are each required for full transcriptional enhancer activity. In contrast, deletion of the T beta 1- and T beta 5-binding sites had essentially no effect on enhancer function. Electrophoretic mobility shift assays demonstrated that TCR alpha/beta + and TCR gamma/delta + T cells expressed T beta 2-, T beta 3-, and T beta 4-binding activities. In contrast, non-T-cell lines, in which the enhancer was inactive, each lacked expression of at least one of these binding activities. TCR alpha and beta gene expression may be regulated by a common set of T-cell nuclear proteins in that the T beta 2 element binding a set of cyclic AMP response element-binding proteins that are also bound by the T alpha 1 element of the human TCR alpha enhancer and the decamer element present in a large number of human and murine TCR beta promoters. Similarly, the T beta 5 TCR beta-enhancer element and the T alpha 2 TCR alpha-enhancer element bind at least one common T-cell nuclear protein. Taken together, these results suggest that TCR beta gene expression is regulated by the interaction of multiple T cell nuclear proteins with a transcriptional enhancer element located 3' of the C beta 2 gene and that some of these proteins may be involved in the coordinate regulation of TCR alpha and beta gene expression.
|
pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2153177,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2156339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2426193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2493990,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2522500,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2524381,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2557542,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2578321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-271968,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2753913,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2761540,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2788889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2838755,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2847918,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2875459,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2965094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2968651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-2983227,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3023965,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3029703,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3034432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3034433,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3043226,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3050531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3092224,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3144478,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3259318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3265470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3317824,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3396541,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3476959,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3487737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3491297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3499667,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3755221,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3871511,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-3919308,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-6208306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-6246368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-6960240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2144610-6982759
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0270-7306
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
10
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
5486-95
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:2144610-Base Sequence,
pubmed-meshheading:2144610-Binding Sites,
pubmed-meshheading:2144610-Cell Line,
pubmed-meshheading:2144610-DNA Mutational Analysis,
pubmed-meshheading:2144610-Enhancer Elements, Genetic,
pubmed-meshheading:2144610-Humans,
pubmed-meshheading:2144610-Molecular Sequence Data,
pubmed-meshheading:2144610-Nuclear Proteins,
pubmed-meshheading:2144610-Oligonucleotides,
pubmed-meshheading:2144610-Promoter Regions, Genetic,
pubmed-meshheading:2144610-Receptors, Antigen, T-Cell,
pubmed-meshheading:2144610-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:2144610-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:2144610-Transcription, Genetic
|
pubmed:year |
1990
|
pubmed:articleTitle |
Identification and functional characterization of the human T-cell receptor beta gene transcriptional enhancer: common nuclear proteins interact with the transcriptional regulatory elements of the T-cell receptor alpha and beta genes.
|
pubmed:affiliation |
Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor 48109-0650.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|