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Titolo:
Isoquinolinesulphonamide derivatives inhibit transcriptional elongation ofhuman immunodeficiency virus type 1 RNA in a promyelocytic model of latency
Autore:
Critchfield, JW; Ho, O; Roberts, BD; Van Lint, C; Verdin, E; Butera, ST;
Indirizzi:
Ctr Dis Control & Prevent, HIV & Retrovirol Branch, Div AIDS STD & TD Lab REs, Natl Ctr Infect Dis, Atlanta, GA 30333 USA Ctr Dis Control & Prevent Atlanta GA USA 30333 Dis, Atlanta, GA 30333 USA Free Univ Brussels, B-1640 Rhode St Genese, Belgium Free Univ Brussels Rhode St Genese Belgium B-1640 ode St Genese, Belgium Univ Calif San Francisco, Gladstone Inst Virol & Immunol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
ANTIVIRAL CHEMISTRY & CHEMOTHERAPY
fascicolo: 5, volume: 10, anno: 1999,
pagine: 275 - 284
SICI:
0956-3202(199909)10:5<275:IDITEO>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; PROTEIN-KINASE-C; ACTIVE ANTIRETROVIRAL THERAPY; LONG TERMINAL REPEAT; HIV-1 REPLICATION; GENE-EXPRESSION; IN-VITRO; CHRONIC INFECTION; CELL-LINES;
Keywords:
HIV-1 latency; transcriptional inhibitors; cellular factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Butera, ST Ctr Dis Control & Prevent, HIV & Retrovirol Branch, Div AIDS STD & TD Lab REs, Natl Ctr Infect Dis, 1600 Clifton Rd NE,Mailstop G-19, Atlanta, GA 30333 USA Ctr Dis Control & Prevent 1600 Clifton Rd NE,Mailstop G-19 Atlanta GA USA 30333
Citazione:
J.W. Critchfield et al., "Isoquinolinesulphonamide derivatives inhibit transcriptional elongation ofhuman immunodeficiency virus type 1 RNA in a promyelocytic model of latency", ANTIVIR CHE, 10(5), 1999, pp. 275-284

Abstract

Using the OM-10.1 promyelocytic model of inducible human immunodeficiency virus type 1 (HIV-1) infection, we tested a panel of known protein kinase inhibitors for an ability to block tumour necrosis factor-alpha-induced HIV-1 expression. Among the compounds tested, the broad-spectrum protein kinaseinhibitor H-7 uniquely blocked HIV-1 expression at the level of viral transcription, but did not inhibit nuclear factor kappa B activation or function. In structure-activity analysis this inhibitory activity of H-7 on HIV-1 expression corresponded with the known structural requirements for the interaction of H-7 with the ATP-binding region of protein kinase C, suggesting that it was indeed related to the kinase inhibitory properties of H-7. The mechanism of H-7 transcriptional inhibition did not involve chromatin remodelling at the HIV-1 long terminal repeat promoter, as shown by nuc-1 disruption, and appeared to involve HIV-1 RNA elongation but not initiation. Therefore, H-7 and related isoquinoline-sulphonamide analogues are most likely inhibiting a kinase target essential for HIV-1 transcriptional elongation whose identity may provide new therapeutic targets for intervention.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 23:24:07