Characterization of interactions between transcription factors and a regulatory region spanning nt-320 to-281 of the HIV-1 LTR in T-lymphoid and non-T-lymphoid cells
- Author(s)
- Pereira, LA; Churchill, MJ; Elefanty, AG; Gouskos, T; Lambert, PF; Ramsay, RG; Deacon, NJ;
- Details
- Publication Year 2002-01,Volume 9,Issue #1,Page 68-81
- Journal Title
- JOURNAL OF BIOMEDICAL SCIENCE
- Publication Type
- Journal Article
- Abstract
- HIV-1 gene expression is regulated by the interplay of transcription factors with multiple binding motifs present within the U3, R and U5 regions of the long terminal repeat (LTR). Here we report novel DNA binding complexes (termed 9a, 9b and 9c) between nuclear proteins from T-lymphoid and non-T-lymphoid cells and a region of the U3 LTR between nucleotides (nts) -320 to -281 in the HIV strain HXB2. Complex 9b bound a motif predicted to bind E-box or c-Myb proteins and a partially overlapping dyad symmetrical motif, and included basic helix-loop-helix proteins (E12, E47 or ITF-1) but surprisingly not c-Myb. Complex 9c, which bound to a pair of GATA sites, included GATA-3 and GATA-4 in Jurkat and MT-2 cells, respectively. We also demonstrate that the c-Myb/E-box and GATA sites form a bipartite motif required for the formation of complex 9a. Transient transfection experiments with T cells revealed that in the context of a minichromosome assembled full-length LTR, mutation of region -320 to -281 increased basal and PMA-stimulated LTR activity. These findings suggest that this region is an important component of the HIV-1 LTR required for response to different cellular transcription factors. Copyright (C) 2002 National Science Council, ROC and S. Karger AG, Basel.
- Publisher
- KARGER
- Keywords
- IMMUNODEFICIENCY-VIRUS TYPE-1; LONG TERMINAL REPEAT; GATA-BINDING PROTEINS; ONCOGENE PRODUCT; IN-VITRO; C-MYB; EXPRESSION; ACTIVATION; ENHANCER; ELEMENT
- Publisher's Version
- https://doi.org/10.1007/BF02256580
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2002-01-01 12:00:00