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Titolo:
Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation
Autore:
Jin, DY; Wang, HL; Zhou, Y; Chun, ACS; Kibler, KV; Hou, YD; Kung, HF; Jeang, KT;
Indirizzi:
NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA NIAID Bethesda MD USA 20892 ol Microbiol Lab, NIH, Bethesda, MD 20892 USA Chinese Acad Prevent Med, Inst Virol, Natl Key Lab Mol Virol & Genet Engn,Beijing 100052, Peoples R China Chinese Acad Prevent Med Beijing Peoples R China 100052 Peoples R China Univ Hong Kong, Inst Mol Biol, Hong Kong, Hong Kong, Peoples R China Univ Hong Kong Hong Kong Hong Kong Peoples R China Kong, Peoples R China
Titolo Testata:
EMBO JOURNAL
fascicolo: 4, volume: 19, anno: 2000,
pagine: 729 - 740
SICI:
0261-4189(20000215)19:4<729:HCVCPL>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
LYMPHOTOXIN-BETA RECEPTOR; RAT EMBRYO FIBROBLASTS; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION FACTORS; SUBCELLULAR-LOCALIZATION; NUCLEAR-LOCALIZATION; PROMOTER ACTIVITY; TRANSGENIC MICE; EXPRESSION; APOPTOSIS;
Keywords:
bZIP transcription factor; hepatitis C virus; hepatitis C virus core protein; hepatocellular carcinoma; LZIP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
88
Recensione:
Indirizzi per estratti:
Indirizzo: Jin, DY NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA NIAID Bethesda MD USA 20892 biol Lab, NIH, Bethesda, MD 20892 USA
Citazione:
D.Y. Jin et al., "Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation", EMBO J, 19(4), 2000, pp. 729-740

Abstract

Hepatitis C virus (HCV) is the major etiological agent of blood-borne non-A non-B hepatitis and a leading cause of liver cirrhosis and hepatocellularcarcinoma worldwide. HCV core protein is a multifunctional protein with regulatory functions in cellular transcription and virus-induced transformation and pathogenesis. Here we report on the identification of a bZIP nucleartranscription protein as an HCV core cofactor for transformation. This bZIP factor, designated LZIP, activates CRE-dependent transcription and regulates cell proliferation. Loss of LZIP function in NIH 3T3 cells triggers morphological transformation and anchorage-independent growth. We show that HCV core protein aberrantly sequesters LZIP in the cytoplasm, inactivates LZIP function and potentiates cellular transformation. Our findings suggest that LZIP might serve a novel cellular tumor suppressor function that is targeted by the HCV core.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 14:30:31