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HIV-I TAT inhibits PKR activity by both RNA-dependent and RNA-independent mechanisms.

Abstract：

:Replication of the human immunodeficiency virus type 1 (HIV-1) is inhibited by interferons (IFNs), in part through activity of the IFN-inducible protein kinase PKR. To escape this antiviral effect, HIV-1 has developed strategies for blocking PKR function. We have previously shown that the HIV-1 Tat protein can associate with PKR in vitro and in vivo and inhibit PKR activity. Here we present evidence that Tat can inhibit PKR activity by both RNA-dependent and RNA-independent mechanisms. Tat inhibited PKR activation by the non-RNA activator heparin, and also suppressed PKR basal level autophosphorylation in the absence of RNA. However, when Tat and dsRNA were preincubated, the amount of Tat required to inhibit PKR activation by dsRNA depended on the dsRNA concentration. In addition to its function in vitro, Tat can also reverse translation inhibition mediated by PKR in COS cells. The Tat amino acid sequence required for interaction with PKR was mapped to residues 40-58, overlapping the hydrophobic core and basic region of HIV-1 Tat. Alignment of amino acid sequences of Tat and eIF-2alpha indicates similarity between the Tat-PKR binding region and the residues around the eIF-2alpha phosphorylation site, suggesting that Tat and eIF-2alpha may bind to the same site on PKR.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Cai R,Carpick B,Chun RF,Jeang KT,Williams BR

doi

10.1006/abbi.1999.1583

subject

Has Abstract

pub_date

2000-01-15 00:00:00

pages

361-7

issue

2

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(99)91583-7

journal_volume

373

pub_type

杂志文章

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