PubMed:1987353
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/1987353","sourcedb":"PubMed","sourceid":"1987353","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/1987353","text":"The NF kappa B independent cis-acting sequences in HIV-1 LTR responsive to T-cell activation.\nThe rate of transcription initiation directed by the long terminal repeat (LTR) of HIV-1 increases in response to mitogenic stimuli of T cells. Here we show that the response of the HIV-1 LTR may be governed by two independent sequences located 5' to the site of transcription initiation sequences that bind either NFAT-1 or NF kappa B. The rate of LTR-directed gene expression increased in response to treatment with either a phorbol ester or tumor necrosis factor alpha if either the NFAT-1 or NF kappa B binding sites were deleted, but failed to respond to these mitogenic stimuli if both sequences were absent. The HIV-1 mutant virus containing both NF kappa B and NFAT-1 deletion was able to replicate although at a much decreased growth rate, while the deletion of NFAT-1 alone increased the viral growth rate in Jurkat cells. Neither deletion of NF kappa B nor deletion of NFAT-1 decreased activation of viral replication by phorbol 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