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Title: Karyopherin {beta}3: A new cellular target for the HPV-16 E5 oncoprotein

Epidemiological and experimental studies have shown that high-risk human papillomaviruses (HPVs) are the causative agents of cervical cancer worldwide, and that HPV-16 is associated with more than half of these cases. In addition to the well-characterized E6 and E7 oncoproteins of HPV-16, recent evidence increasingly has implicated the HPV-16 E5 protein (16E5) as an important mediator of oncogenic transformation. Since 16E5 has no known intrinsic enzymatic activity, its effects on infected cells are most likely mediated by interactions with various cellular proteins and/or its documented association with lipid rafts. In the present study, we describe a new cellular target that binds to 16E5 in COS cells and in stable human ectocervical cell lines. This target is karyopherin {beta}3, a member of the nuclear import receptor family with critical roles in the nuclear import of ribosomal proteins and in the secretory pathway.
Authors:
 [1] ;  [2] ;  [1] ;  [3]
  1. Department of Pathology, Georgetown University Medical School, 3900 Reservoir Road NW, Washington, DC 20057 (United States)
  2. Laboratory of Cell Biochemistry and Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 (United States)
  3. Department of Pathology, Georgetown University Medical School, 3900 Reservoir Road NW, Washington, DC 20057 (United States), E-mail: suprynfa@georgetown.edu
Publication Date:
OSTI Identifier:
21143751
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 371; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2008.04.122; PII: S0006-291X(08)00795-X; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; HEALTH HAZARDS; LIPIDS; NEOPLASMS; ONCOGENIC TRANSFORMATIONS; RECEPTORS