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September 1, 1989Journal of Biological ChemistryOpen Access

HTLV-I tax gene product activates transcription via pre-existing cellular factors and cAMP responsive element

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Authors

CGChou‐Zen GiamUniformed Services University of the Health SciencesYXYinzhe XuState Grid Corporation of China (China)

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Overview

Molecular study demonstrates HTLV-I Tax trans-activates viral LTR through cAMP responsive elements in host cells, indicating Tax acts indirectly via pre-existing cellular transcription factors.

Key Points

  • To determine whether HTLV-I Tax protein directly binds viral regulatory sequences or requires host cellular factors to trans-activate transcription.
  • Assessed Tax-mediated HTLV-I long terminal repeat (LTR) trans-activation in the absence of de novo cellular protein synthesis.
  • Performed saturated mutagenesis across the viral 21-base pair repeats containing the cAMP responsive element motif.
  • Tested purified Tax protein for direct binding activity to the 21-base pair repeat sequences and nonspecific DNA.
  • Tax protein induced LTR trans-activation without requiring new cellular protein synthesis, demonstrating dependence on pre-existing host factors.
  • Mutations localized exclusively within the 5' six bases of the cAMP responsive element (TGACGTCA) completely abolished Tax-mediated trans-activation.
  • Purified Tax protein showed no direct binding affinity to the 21-base pair repeats or nonspecific DNA, indicating activation occurs through intermediary cellular proteins.

Cite This Study

Giam et al. (1989) studied this question.

synapsesocial.com/papers/6a75a3b2dcfefe9676dd8652https://doi.org/10.1016/s0021-9258(19)84815-9
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