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Titolo:
Alterations in HIV-1 Rev transport in response to cell stress
Autore:
Soros, V; Cochrane, A;
Indirizzi:
Univ Toronto, Dept Med Genet & Microbiol, Toronto, ON M5S 1A8, Canada UnivToronto Toronto ON Canada M5S 1A8 obiol, Toronto, ON M5S 1A8, Canada
Titolo Testata:
VIROLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: 199 - 210
SICI:
0042-6822(20010215)280:2<199:AIHRTI>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; VIRAL MESSENGER-RNA; PROTEIN-KINASE INHIBITORS; NUCLEAR EXPORT SIGNALS; ACTIVATION DOMAIN; GENE-PRODUCT; LEPTOMYCIN-B; STRUCTURED REGION; TARGET SEQUENCE; TYPE-1 AFFECTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Cochrane, A Univ Toronto, Dept Med Genet & Microbiol, 100 Coll St, Toronto, ON M5S 1A8, Canada Univ Toronto 100 Coll St Toronto ON Canada M5S 1A8 1A8, Canada
Citazione:
V. Soros e A. Cochrane, "Alterations in HIV-1 Rev transport in response to cell stress", VIROLOGY, 280(2), 2001, pp. 199-210

Abstract

Movement of HIV-I Rev between the nucleus and cytoplasm is essential to its function. While normally nuclear, the protein can be induced to accumulate in the cytoplasm upon inhibition of RNA polymerase I/II. Nuclear accumulation of Rev in the presence of these inhibitors was found to be rescued upon addition of leptomycin B, an inhibitor of Rev nuclear export. This finding. in conjunction with kinetic data on nuclear import, indicates that the effect of the RNA polymerase inhibitors is due to an inversion of the rates of nuclear import versus export possibly achieved by increasing the rate ofRev nuclear export. We also examined whether changes in Rev localization could be due to a stress response. While neither ultraviolet radiation nor heat shock affected Rev subcellular localization, both oxidative and osmoticshocks induce changes in Rev localization comparable to that observed withthe RNA polymerase inhibitors. The ability of certain serine/threonine kinase inhibitors. including CKI/II inhibitors, to cause cytoplasmic accumulation of Rev suggested that the alteration in Rev distribution could be due to changes in Rev or CRM1 phosphorylation. However, no change in extent of phosphorylation of either protein is observed upon treatment of cells with any of the agents tested. indicating involvement of another cellular factor. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/10/20 alle ore 00:23:12