| FEBS Letters | |
| p21ras contributes to HIV‐1 activation in T‐cells | |
| Telford, John L.1  Macchia, Giovanni1  Massone, Annalisa1  Baldari, Cosima T.2  | |
| [1] I.R.I.S., Via Fiorentina 1, 53100 Siena, Italy;Department of Evolutionary Biology, University of Siena, Via Mattioli 4, 53100 Siena, Italy | |
| 关键词: HIV-1; Interleukin; Signal transduction; Cyclosporin A; LTR; long terminal repeat; PKC; protein kinase C; CAT; acetyl chloramphenicol transferase; CsA; cyclosporin A; | |
| DOI : 10.1016/0014-5793(92)80633-R | |
| 学科分类:生物化学/生物物理 | |
| 来源: John Wiley & Sons Ltd. | |
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【 摘 要 】
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.
【 授权许可】
Unknown
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO201912020296427ZK.pdf | 514KB |
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