Abstract:
:Activation of T-cells infected by HIV-1 results in activation of long terminal repeat (LTR)-dependent viral transcription and ultimately the production of infectious virus. Although full T-cell activation requires a complex series of intracellular signals, including protein kinase C activation, calcium mobilisation, and less-well defined lymphokine-induced signals, the HIV-1 LTR can be activated by subsets of these signals. We have studied the interaction of these signals in the human lymphoma line, Jurkat, in activation of the HIV-1 LTR. The HIV promoter was induced by IL-1 and phorbol ester activation of PKC but not by a calcium ionophore. The constitutively active form of Ha-ras could replace phorbol ester stimulation of the HIV promoter and of a synthetic promoter containing NF kappa B binding sites.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Baldari CT,Macchia G,Massone A,Telford JLdoi
10.1016/0014-5793(92)80633-rkeywords:
subject
Has Abstractpub_date
1992-06-15 00:00:00pages
261-4issue
2-3eissn
0014-5793issn
1873-3468pii
0014-5793(92)80633-Rjournal_volume
304pub_type
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