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Titolo:
Inhibition of human immunodeficiency virus type 1 Rev function by a dominant-negative mutant of Sam68 through sequestration of unspliced RNA at perinuclear bundles
Autore:
Soros, VB; Carvajal, HV; Richard, S; Cochrane, AW;
Indirizzi:
Univ Toronto, Dept Med & Mol Genet & Microbiol, Toronto, ON M5S 1A8, Canada Univ Toronto Toronto ON Canada M5S 1A8 obiol, Toronto, ON M5S 1A8, Canada Lady Davis Inst Med Res, Terry Fox Mol Oncol Grp, Montreal, PQ, Canada Lady Davis Inst Med Res Montreal PQ Canada col Grp, Montreal, PQ, Canada McGill Univ, Montreal, PQ H3T 1E2, Canada McGill Univ Montreal PQ Canada H3T 1E2 Univ, Montreal, PQ H3T 1E2, Canada
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 17, volume: 75, anno: 2001,
pagine: 8203 - 8215
SICI:
0022-538X(200109)75:17<8203:IOHIVT>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
VIRAL MESSENGER-RNA; NUCLEAR EXPORT SIGNALS; HIV-1 REV; TRANS-ACTIVATOR; KH-DOMAIN; REGULATED EXPRESSION; STRUCTURED REGION; POLYMERASE-II; GENE-PRODUCT; CELL-LINES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Cochrane, AW Univ Toronto, Dept Med & Mol Genet & Microbiol, 100 Coll St, Toronto, ON M5S 1A8, Canada Univ Toronto 100 Coll St Toronto ON Canada M5S 1A8 A8, Canada
Citazione:
V.B. Soros et al., "Inhibition of human immunodeficiency virus type 1 Rev function by a dominant-negative mutant of Sam68 through sequestration of unspliced RNA at perinuclear bundles", J VIROLOGY, 75(17), 2001, pp. 8203-8215

Abstract

Human immunodeficiency virus (HIV) type 1 encodes an essential protein, Rev, which functions to transport unspliced and singly spliced viral transcripts from the nucleus to the cytoplasm to allow expression of the viral structural proteins. It has previously been reported that Sam68 synergisticallystimulates Rev activity (T. Reddy et al., Nat. Med. 5:635-642, 1999). Herewe report that the Sam68-like mammalian proteins SLM1 and SLM2 also stimulate Rev activity. Their stimulation ability cannot be attributed to a shuttling property, since Sam68, SLM1, and SLM2 do not display significant shuttling activity alone or in the presence of Rev. In addition, Sam68, SLM1, and SLM2 do not affect the equilibrium between unspliced and completely spliced HIV RNA. The C-terminally truncated Sam68 mutant (Sam68 DeltaC) previously observed to inhibit the Sam68-mediated stimulation of Rev activity (Reddy et al., 1999) also inhibits SLM1- and SLM2-mediated stimulation of Rev activity. This suggests that the mechanism by which Sam68, SLM1, and SLM2 stimulate Rev activity may be common. Sam68 DeltaC does not inhibit Rev activity by inhibiting Rev from shuttling between the nucleus and cytoplasm. Inhibition by Sam68 DeltaC is a consequence of its mislocalization to the cytoplasm, as evidenced by the fact that addition of an exogenous nuclear localization signal to Sam68 DeltaC restores nuclear localization and stimulationof Rev activity. We demonstrate that Sam68 DeltaC causes perinuclear accumulation of unspliced HIV env RNA and propose that Sam68 DeltaC inhibits Revactivity by sequestering Rev-responsive RNA away from the translation apparatus.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 02:07:33