E7 proteins from high- and low-risk human papillomaviruses bind to TGF-β-regulated Smad proteins and inhibit their transcriptional activity

E7 proteins from high- and low-risk human papillomaviruses bind to TGF-β-regulated Smad proteins... Human papillomaviruses (HPV) infect keratinocytes of skin and mucosa. Persistent infection can lead to the formation of benign tumors. In cases of high-risk HPV, such as HPV16 or 18, these may further progress to cancer. In order to support viral replication in suprabasal keratinocytes, the HPV E7 protein employs various strategies to keep keratinocytes in cycle and counteracts anti-proliferative signals from outside. HPV16 E7 can directly interfere with transforming growth factor-β (TGF-β) signalling by binding to Smad proteins mediating growth arrest. It has been speculated that this property of HPV16 E7 contributes to HPV-associated carcinogenesis. Here, we show that E7 proteins from different low- and high-risk HPV types bind to Smad 1 to 4. The E7 protein from HPV1, a low-risk HPV causing plantar warts, efficiently inhibited Smad 3-induced transcription. Our data strongly indicate that the Smad-binding capacity of E7 proteins from different HPVs may preserve keratinocyte proliferation required for the productive viral life cycle rather than promoting carcinogenesis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

E7 proteins from high- and low-risk human papillomaviruses bind to TGF-β-regulated Smad proteins and inhibit their transcriptional activity

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Publisher
Springer-Verlag
Copyright
Copyright © 2006 by Springer-Verlag
Subject
Biomedicine; Medical Microbiology; Virology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-006-0768-1
Publisher site
See Article on Publisher Site

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