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p21 ras contributes to HIV‐1 activation in T‐cells
Author(s) -
Baldari Cosima T.,
Macchia Giovanni,
Massone Annalisa,
Telford John L.
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)80633-r
Subject(s) - human immunodeficiency virus (hiv) , chemistry , virology , microbiology and biotechnology , biology
Activation of T‐cells infected by HIV‐1 results in activation of long terminal repeal (LTR)‐dependent viral transcription and ultimately the production of infectious virus. Although fulI 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 NFκB binding sites.