Overexpression of TAR sequences renders cells resistant to human immunodeficiency virus replication

Sullenger, Bruce A.; Gallardo, Humilidad F.; Ungers, Grace; Gilboa, Eli

doi:10.1016/0092-8674(90)90455-n

Cited by 426 publications

(248 citation statements)

References 33 publications

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“…14,21,22,36,[38][39][40]42,43,45 However, control elements known as locus control regions (LCRs) have been shown to confer high level tissue specific, chromosomal position independent expression. 47 In the case of the human ␤-globin locus LCR, high level, erythroid-specific expression is obtained.…”

Section: Resultsmentioning

confidence: 99%

“…Decoys such as TAR 21 and RRE 22 could inhibit the action of Tat and Rev regulatory proteins in HIV replication by sequestering these RNA binding proteins. TAR RNA from HIV-1 forms a stable stem-loop structure (from +1 to +60), the maintenance of which is critical for Tatmediated transactivation.…”

Section: Introductionmentioning

confidence: 99%

“…29,30 To date, several studies have shown the inhibition of HIV replication by the expression of either TAR or RRE RNA decoy sequences. 21,22,31,32 Another category of RNA inhibitor consists of HIV RNA specific ribozymes. Ribozymes are described as catalytic RNA molecules capable of recognizing and cleaving a specific target RNA.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

High level inhibition of HIV replication with combination RNA decoys expressed from an HIV-Tat inducible vector

Fraisier

Irvine²,

Wrighton³

et al. 1998

Gene Ther

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

High level inhibition of HIV replication with combination RNA decoys expressed from an HIV-Tat inducible vector

Fraisier

Irvine²,

Wrighton³

et al. 1998

Gene Ther

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“…It blocks the binding of nuclear factors to promoter regions of targeted genes, resulting in inhibition of gene transactivation in vitro and in vivo. 21,22 Such a decoy strategy has been proposed for the treatment of some human diseases represented by animal models. 23,24 Recently, we developed decoy ciselements oligo deoxyribonucleic acid against NFkB (NFkB-decoy), which inhibited the production of major inflammatory cytokines and expression of adhesion molecules in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

Transfection of NFκB-decoy oligodeoxynucleotides using efficient ultrasound-mediated gene transfer into donor kidneys prolonged survival of rat renal allografts

et al. 2003

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Nuclear factor kB (NFkB) plays a pivotal role in the coordinated transactivation of a series of genes of cytokines and adhesion molecules that are highly involved in the onset of acute rejection in organ transplantation. We previously developed decoy cis-elements oligo deoxyribonucleic acid against NFkB (NFkB-decoy) that effectively inhibited the activation of major inflammatory mediators in vitro and in vivo. Accordingly, we hypothesized that transfection of NFkB-decoy into the donor kidney would prevent acute rejection and prolong graft survival, and thus provide effective therapy for renal acute rejection. To transfect NFkB-decoy, we employed a novel approach using ultrasound exposure with an echocardiographic contrast agent, Optison, and clearly demonstrated successful transfection of NFkB-decoy into renal tissue. The therapeutic effect of NFkB-decoy on renal allografts was then evaluated in a rat renal allograft model (Wistar-Lewis). In the control group, graft function significantly deteriorated with marked destruction of renal tissue, accompanied by increased production of major inflammatory mediators, and all animals died of renal failure by 9 days. In contrast, graft function (serum creatinine on day 2, NFkB-treated: 0.9770.16 versus control: 1.8470.23 mg/dl, Po0.01) and histological structure were well preserved with significantly decreased expression of NFkB-regulated cytokines and adhesion molecules, including IL-1, iNOS, MCP-1, TNF-a, and ICAM-1, in allografts transfected with NFkB-decoy. As a result, animal survival was significantly prolonged in this group as compared to controls (14.275.2 versus 7.171.2 days, Po0.01). Thus, we established a novel ultrasound-Optison-mediated gene transfection approach and demonstrated the significant prolongation of graft survival by the successful transfection of NFkB-decoy into the donor kidney in a rat renal allograft model. Gene Therapy (2003) 10, 415-425.

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“…To date, several RNA and protein agents have been introduced into susceptible cells and tested as inhibitors of HIV-1 replication. These studies have included dominant negative mutants of HIV structural (Gag, 1 Env 2 ) or regulatory (Rev, 3 Tat, 4 PR 5 ) proteins, TAR 6 and RRE 7 RNA decoys molecules for the viral proteins (Tat, REV), antisense RNAs, 8 antibodies directed against Rev, 9 gp120 10 or Tat, 11 and ribozyme designed to cleave at different conserved sites of the HIV-1 genome. 12,13 These approaches all target phases of HIV-1 replication before virus assembly.…”

Section: Introductionmentioning

confidence: 99%

HIV-1 proprotein processing as a target for gene therapy

2003

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Overexpression of TAR sequences renders cells resistant to human immunodeficiency virus replication

Cited by 426 publications

References 33 publications

High level inhibition of HIV replication with combination RNA decoys expressed from an HIV-Tat inducible vector

High level inhibition of HIV replication with combination RNA decoys expressed from an HIV-Tat inducible vector

Transfection of NFκB-decoy oligodeoxynucleotides using efficient ultrasound-mediated gene transfer into donor kidneys prolonged survival of rat renal allografts

HIV-1 proprotein processing as a target for gene therapy

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