| Autor: |
Jin DY; Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0460, USA. dyjin@hkucc.hku.hk, Wang HL, Zhou Y, Chun AC, Kibler KV, Hou YD, Kung H, Jeang KT |
| Jazyk: |
angličtina |
| Zdroj: |
The EMBO journal [EMBO J] 2000 Feb 15; Vol. 19 (4), pp. 729-40. |
| DOI: |
10.1093/emboj/19.4.729 |
| Abstrakt: |
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 hepatocellular carcinoma 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 nuclear transcription 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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