You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
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
You can always find the topics here!Topics: Taxes, Antibodies, Human T lymphotropic virus 1, Gels, DNA, T lymphocytes, Transactivation, Proteins, Phosphorylation, Biochemistry
Were these topics helpful?See somethings inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
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