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Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation.


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 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.

SUBMITTER: Jin DY 

PROVIDER: S-EPMC305611 | biostudies-literature | 2000 Feb

REPOSITORIES: biostudies-literature

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Hepatitis C virus core protein-induced loss of LZIP function correlates with cellular transformation.

Jin D Y DY   Wang H L HL   Zhou Y Y   Chun A C AC   Kibler K V KV   Hou Y D YD   Kung H H   Jeang K T KT  

The EMBO journal 20000201 4


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  ...[more]

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