Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunopurified TFIID produces a large DNase I footprint over the hsp70, hsp26, and histone H3 promoters of Drosophila. These footprints span from the TATA element to a position approximately 35 nucleotides downstream from the transcription start site. Using a "missing nucleoside" analysis, four regions within the three promoters have been found to be important for TFIID binding: the TATA element, the initiator, and two regions located approximately 18 and 28 nucleotides downstream of the transcription start site. On the basis of the missing nucleoside data, the initiator appears to contribute as much to the affinity as the TATA element. However, there is weak conservation of the sequence in this region. To determine whether a preferred binding sequence exists in the vicinity of the initiator, the nucleotide composition of this region within the hsp70 promoter was randomized and then subjected to selection by TFIID. After five rounds of selection, the preferred sequence motif--G/A/T C/TAT/GTG--emerged. This motif is a close match to consensus sequences that have been derived by comparing the initiator region of numerous insect promoters. Selection of this sequence demonstrates that sequence-specific interactions downstream of the TATA element contribute to the interaction of TFIID on a wide spectrum of promoters.
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PMID:TFIID sequence recognition of the initiator and sequences farther downstream in Drosophila class II genes. 792 71

Here we demonstrate that an inducible anti-HIV short hairpin RNA (shRNA) expressed from a Pol II promoter inhibits HIV-1 gene expression in mammalian cells. Our strategy is based on a promoter system in which the HIV-1 LTR is fused to the Drosophila hsp70 minimal heat shock promoter. This system is inducible by HIV-1 TAT, which functions in a negative feedback loop to activate transcription of an shRNA directed against HIV-1 rev. Upon induction the shRNA is processed to an siRNA that guides inhibition of HIV replication in cultured T-lymphocytes and hematopoietic stem cell-derived monocytes. The fusion promoter system may be safer than drug-inducible systems for shRNA-mediated gene therapy against HIV as the shRNAs are only expressed following HIV infection.
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PMID:Negative feedback inhibition of HIV-1 by TAT-inducible expression of siRNA. 1556 18