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Human T-Cell Lymphotropic Virus Type I (HTLV-I) Transcriptional Activator, Tax, Enhances CREB Binding to HTLV-I 21-Base-Pair Repeats by Protein-Protein Interaction
Ling-Jun Zhao and Chou-Zen Giam
Proceedings of the National Academy of Sciences of the United States of America
Vol. 89, No. 15 (Aug. 1, 1992), pp. 7070-7074
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2359933
Page Count: 5
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HTLV-I Tax protein activates transcription from three 21-base-pair (bp) repeat sequences in the viral enhancer. The HTLV-I 21-bp repeat contains a TGACGT motif that is homologous to the cAMP-responsive element (CRE) and crucial for tax transactivation. Tax exhibits marginal affinity for DNA but rather interacts with cellular CRE-binding proteins to enhance their affinity for the HTLV-I 21-bp repeats. Using the HTLV-I 21-bp repeat and Jurkat T-lymphocyte nuclear extract in a gel electrophoretic mobility-shift assay, we previously detected three protein-DNA complexes that are specific for the CRE in the 21-bp repeat (complexes I, II, and IV). Complexes I and II but not IV interacted with Tax. We now show that complexes I, II, and IV are composed of CREB (CRE binding protein) homodimer, CREB/ATF-1 (activating transcription factor 1) heterodimer, and ATF-1 homodimer, respectively. Tax stabilizes complexes I and II via a direct interaction with the CREB moiety. In the absence of DNA, CREB and Tax continue to form a complex that can be immunoprecipitated by a Tax-specific antibody. These results suggest that one mechanism by which Tax activates transcription may be mediated through the direct interaction with CREB homodimer and/or CREB/ATF-1 heterodimer to stabilize their assembly on the Tax-responsive CRE motifs in the HTLV-I enhancer.
Proceedings of the National Academy of Sciences of the United States of America © 1992 National Academy of Sciences