We have overexpressed the HIV-1 tat and the HTLV-I tax proteins using an eucaryotic baculovirus-insect cell system. In analyzing the molecular mechanism(s) of tat and tax, we have noted the following salient observations: 1) neither tat or tax appears to function through direct binding to its respective target sequence in the viral LTR; 2) activation of the respective LTRs by the HIV-1 tat or the HTLV-1 tax proteins occurs in the absence of de novo cellular protein synthesis; 3) tax activates the HTLV-1 LTR through a set of triply-repeated 21 bp sequences which contain a consensus cAMP-responsive motif; and 4) a number of host cell proteins specifically bind to the HIV-1 TAR RNA sequence element. Our current working hypothesis is that activation of the HIV-1/HTLV-1 LTR is mediated through functional interactions between preexisting cellular transcription factors and the viral trans-activator proteins.
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Grassmann, Ralph; Jeang, Kuan-Teh (2008) The roles of microRNAs in mammalian virus infection. Biochim Biophys Acta : |
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Lee, Jia Hai; Yedavalli, Venkat Rk; Jeang, Kuan-Teh (2007) Activation of HIV-1 expression and replication by cGMP dependent protein kinase type 1-beta (PKG1beta). Retrovirology 4:91 |
Berkhout, Ben; Jeang, Kuan-Teh (2007) RISCy business: MicroRNAs, pathogenesis, and viruses. J Biol Chem 282:26641-5 |
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Yeung, Man Lung; Benkirane, Monsef; Jeang, Kuan-Teh (2007) Small non-coding RNAs, mammalian cells, and viruses: regulatory interactions? Retrovirology 4:74 |
Yedavalli, Venkat R K; Jeang, Kuan-Teh (2007) Methylation: a regulator of HIV-1 replication? Retrovirology 4:9 |
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