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CCAAT/enhancer-binding proteins modulate human T cell leukemia virus type 1 long terminal repeat activation
Journal article   Open access   Peer reviewed

CCAAT/enhancer-binding proteins modulate human T cell leukemia virus type 1 long terminal repeat activation

Christian Grant, Michael Nonnemacher, Pooja Jain, Devanshi Pandya, Bryan Irish, Simon C Williams and Brian Wigdahl
Virology (New York, N.Y.), v 348(2), pp 354-369
2006
PMID: 16458341
url
https://doi.org/10.1016/j.virol.2005.12.024View
Published, Version of Record (VoR) Open

Abstract

Monocyte–macrophage HAM/TSP HTLV-1 Tax CCAAT/enhancer-binding protein Long terminal repeat
CCAAT/enhancer-binding protein (C/EBP) basic region/leucine zipper (bZIP) transcription factors have been shown to form heterodimers with cAMP-responsive element binding protein 2 (CREB-2), a transcription factor involved in regulating basal and Tax-mediated transactivation of the human T cell leukemia virus type 1 (HTLV-1) long terminal repeat (LTR). In cells of the monocyte–macrophage lineage (proposed to play a role in HTLV-1 pathogenesis as an accessory target cell), several members of the C/EBP family are expressed at high levels and may have functional impact on both basal and Tax-mediated transactivation of the HTLV-1 LTR. Basal activation of the HTLV-1 LTR was enhanced by overexpression of C/EBPβ, C/EBPδ, or C/EBPε, whereas transactivation of the LTR by Tax was inhibited by overexpression of C/EBPα and C/EBPβ. Inhibition of Tax-mediated transactivation of the HTLV-1 LTR was co-activator-independent, did not require C/EBP binding to the Tax-responsive elements, and may involve heterodimerization with CREB factors.

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Collaboration types
Domestic collaboration
Web of Science research areas
Virology
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