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Titolo:
Sindbis virus entry into cells triggers apoptosis by activating sphingomyelinase, leading to the release of ceramide
Autore:
Jan, JT; Chatterjee, S; Griffin, DE;
Indirizzi:
Johns Hopkins Univ, Sch Hyg & Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA21205 mmunol, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA Johns Hopkins Univ Baltimore MD USA 21287 Pediat, Baltimore, MD 21287 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 14, volume: 74, anno: 2000,
pagine: 6425 - 6432
SICI:
0022-538X(200007)74:14<6425:SVEICT>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; SEMLIKI FOREST VIRUS; ALPHAVIRUS-INDUCED APOPTOSIS; NF-KAPPA-B; NEUTRAL SPHINGOMYELINASE; ACID SPHINGOMYELINASE; SIGNAL-TRANSDUCTION; MEMBRANE-FUSION; PROTEIN-KINASE; PARTIAL-PURIFICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Griffin, DE Johns Hopkins Univ, Sch Publ Hlth, Dept Mol Microbiol & Immunol, 615 N Wolfe St, Baltimore, MD 21205 USA Johns Hopkins Univ 615 N Wolfe St Baltimore MD USA 21205 5 USA
Citazione:
J.T. Jan et al., "Sindbis virus entry into cells triggers apoptosis by activating sphingomyelinase, leading to the release of ceramide", J VIROLOGY, 74(14), 2000, pp. 6425-6432

Abstract

Sindbis virus (SV) causes acute encephalomyelitis by infecting and inducing the death of neurons. Induction of apoptosis occurs during virus entry and involves acid-induced conformational changes in the viral surface glycoproteins and sphingomyelin (SM)-dependent fusion of the virus envelope with the endosomal membrane. We have studied neuroblastoma cells to determine howthis entry process triggers cell death. Acidic sphingomyelinase was activated during entry followed by activation of neutral sphingomyelinase, SM degradation, and a sustained increase in ceramide. Ceramide-induced apoptosis and SV-induced apoptosis could be inhibited by treatment with Z-VAD-fmk, a caspase inhibitor, and by overexpression of Bcl-2, an antiapoptotic cellular protein. Acid ceramidase, expressed in a recombinant SV, decreased intracellular ceramide and protected cells from apoptosis. The data suggest that acid-induced SM-dependent virus fusion initiates the apoptotic cascade by inducing SM degradation and ceramide release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 01:10:59