Human papillomavirus 16 E5 induces bi-nucleated cell formation by cell–cell fusion

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Human papillomavirus 16 E5 induces bi-nucleated cell formation by cell-cell fusion.

Human papillomaviruses (HPV) 16 is a DNA virus encoding three oncogenes--E5, E6, and E7. The E6 and E7 proteins have well-established roles as inhibitors of tumor suppression, but the contribution of E5 to malignant transformation is controversial. Using spontaneously immortalized human keratinocytes (HaCaT cells), we demonstrate that expression of HPV16 E5 is necessary and sufficient for the f...

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Human Papillomavirus Type 16 E5 Protein as a Therapeutic Target

Cervical cancer is a progressive disease with an onset of one to two decades on average. During the productive replication stage, the Human papillomavirus (HPV) genome is maintained episomally in the infected cervical epithelium and early gene products, including E5, are expressed. Therefore, E5 has a potential to contribute to the HPV-associated carcinogenic process. In invasive malignancies, ...

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Membrane orientation of the human papillomavirus type 16 E5 oncoprotein.

The E5 protein of human papillomavirus type 16 is a small, hydrophobic protein that localizes predominantly to membranes of the endoplasmic reticulum (ER). To define the orientation of E5 in these membranes, we employed a differential, detergent permeabilization technique that makes use of the ability of low concentrations of digitonin to selectively permeabilize the plasma membrane and saponin...

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Human Papillomavirus 16 E5 Modulates the Expression of Host MicroRNAs

Human papillomavirus (HPV) infection is a prerequisite of developing cervical cancer, approximately half of which are associated with HPV type 16. HPV 16 encodes three oncogenes, E5, E6, and E7, of which E5 is the least studied so far. Its roles in regulating replication and pathogenesis of HPV are not fully understood. Here we utilize high-throughput screening to coordinately investigate the e...

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ژورنال

عنوان ژورنال: Virology

سال: 2009

ISSN: 0042-6822

DOI: 10.1016/j.virol.2008.10.011