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- W2146863397 abstract "We have previously shown that human papillomavirus virus-like particles (VLPs) are able to activate the Ras/MAP kinase pathway. Ras can also elicit an anti-apoptotic signal via PI3-kinase so we investigated this further. Here we show that binding of VLPs from HPV types 6b, 18, 31, 35 and BPV1 results in activation of PI3-kinase. Activation was achieved by either L1 or L1/L2 VLPs and was dependent on both VLP–cell interaction and correct conformation of the virus particle. VLP-induced PI3-kinase activity resulted in efficient downstream signaling to Akt and consequent phosphorylation of FKHR and GSK3β. We also present evidence that PV signaling is activated via the α6β4 integrin. These data suggest that papillomaviruses use a common receptor that is able to signal through to Ras. Combined activation of the Ras/MAP kinase and PI3-kinase pathways may be beneficial for the virus by increasing cell numbers and producing an environment more conducive to infection." @default.
- W2146863397 created "2016-06-24" @default.
- W2146863397 creator A5073169676 @default.
- W2146863397 creator A5082327578 @default.
- W2146863397 date "2006-09-01" @default.
- W2146863397 modified "2023-10-16" @default.
- W2146863397 title "Papillomavirus virus-like particles activate the PI3-kinase pathway via alpha-6 beta-4 integrin upon binding" @default.
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- W2146863397 doi "https://doi.org/10.1016/j.virol.2006.05.002" @default.
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