Expression of butyrate response factor 1 in HTLV-1-transformed cells and its transactivation by tax protein

Expression of butyrate response factor 1 in HTLV-1-transformed cells and its transactivation by... Tax oncoprotein of Human T-lymphotropic virus 1 (HTLV-1) has been proposed to dysregulate the expression of a number of cellular genes, many of which play a critical role for cell proliferation. Our initial data demonstrated that the immediate-early gene butyrate response factor 1 ( BRF1 ) was upregulated in HTLV-1-infected cells. The ensuing studies revealed that the effect of Tax was mediated through two transcription elements. The more proximal element, located in the vicinity of TATA box, accounted for the main Tax transactivating effect, and it appeared to be a novel transcription factor-binding site. It involved the CCTCCTC sequence (nt −59/−53, relative to transcription start site) and was dubbed BRF1 Tax-responsive site (BTRS). The cellular protein(s) recruited into the formation of DNA-protein complex at this binding site were not identified. The other element, located further upstream, was a consensus cAMP-responsive site (CRE) TGACGTCA, spanning positions −400 to −393. CRE-binding protein (CREB) was found to mediate the transactivating effect of Tax at this site. Our results present the first evidence that the Tax transactivator has a capability to modulate the expression of BRF1 and that this effect is mediated by CRE and a novel BTRS motifs. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Expression of butyrate response factor 1 in HTLV-1-transformed cells and its transactivation by tax protein

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Publisher
Springer-Verlag
Copyright
Copyright © 2003 by Springer-Verlag/Wien
Subject
LifeSciences
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-003-0114-9
Publisher site
See Article on Publisher Site

Abstract

Tax oncoprotein of Human T-lymphotropic virus 1 (HTLV-1) has been proposed to dysregulate the expression of a number of cellular genes, many of which play a critical role for cell proliferation. Our initial data demonstrated that the immediate-early gene butyrate response factor 1 ( BRF1 ) was upregulated in HTLV-1-infected cells. The ensuing studies revealed that the effect of Tax was mediated through two transcription elements. The more proximal element, located in the vicinity of TATA box, accounted for the main Tax transactivating effect, and it appeared to be a novel transcription factor-binding site. It involved the CCTCCTC sequence (nt −59/−53, relative to transcription start site) and was dubbed BRF1 Tax-responsive site (BTRS). The cellular protein(s) recruited into the formation of DNA-protein complex at this binding site were not identified. The other element, located further upstream, was a consensus cAMP-responsive site (CRE) TGACGTCA, spanning positions −400 to −393. CRE-binding protein (CREB) was found to mediate the transactivating effect of Tax at this site. Our results present the first evidence that the Tax transactivator has a capability to modulate the expression of BRF1 and that this effect is mediated by CRE and a novel BTRS motifs.

Journal

Archives of VirologySpringer Journals

Published: Jan 10, 2003

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