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

نویسندگان

  • D Y Jin
  • H L Wang
  • Y Zhou
  • A C Chun
  • K V Kibler
  • Y D Hou
  • H Kung
  • K T Jeang
چکیده

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.

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عنوان ژورنال:
  • The EMBO journal

دوره 19 4  شماره 

صفحات  -

تاریخ انتشار 2000