Wang, YuKang and Kobori, Joan A. and Hood, Leroy (1993) The ht beta gene encodes a novel CACCC box-binding protein that regulates T-cell receptor gene expression. Molecular and Cellular Biology, 13 (9). pp. 5691-5701. ISSN 0270-7306. http://resolver.caltech.edu/CaltechAUTHORS:WANmcb93
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A gene encoding a novel CACCC box-binding protein that binds to the promoter region of the human T-cell receptor (TCR) V beta 8.1 gene and the mouse TCR alpha gene silencer has been cloned. This gene, termed ht beta, contains four zinc fingers of the class Cys2-X12-His2 that may be responsible for DNA binding and a highly negatively charged region that defines a putative transcriptional activation domain. Analysis of the expression of ht beta mRNA revealed similar expression levels and patterns in various cell lines. The bacterially expressed ht beta protein can bind to the CACCC box in both the human TCR V beta 8.1 gene promoter and the mouse TCR alpha gene silencer. The CACCC box is essential for efficient transcription of the V beta 8.1 promoter. Cotransfection with an ht beta expression plasmid and a reporter vector indicated that ht beta can activate human TCR V beta 8.1 gene transcription. ht beta also is able to counteract the silencing effect of the mouse TCR alpha gene silencer. The CACCC box has been found in almost all V beta 8.1 gene subfamily members and in both TCR alpha and beta gene enhancers in humans and mice. These results suggest that the CACCC box-binding protein may have an important regulatory function for TCR gene expression in alpha beta T cells versus gamma delta T cells.
|Additional Information:||Copyright © 1993 by the American Society for Microbiology. Received 11 January 1993/Returned for modification 31 March 1993/Accepted 3 June 1993 We thank K. C. Cheng, Peter Mathisen, Sally Orr, Wenron Qiu, David Wang, Kangsheng Wang, and Ebrahim Zandi for technical advice during the course of this work. We also thank Jeffrey Leiden for critical comments on this work. We are grateful to Peter Mathisen and Erich Strauss for comments on the manuscript. This work was supported in part by National Institutes of Health grant HG00356. Y.W. also thanks the K. C. Wong Education Foundation, Ltd., Hong Kong, for financial aid.|
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|Deposited On:||19 Mar 2006|
|Last Modified:||26 Dec 2012 08:48|
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