期刊
JOURNAL OF VIROLOGY
卷 80, 期 24, 页码 12420-12424出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02576-05
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Mechanisms of cellular transformation associated with human papillomavirus type 5 (HPV5), which is responsible for skin carcinomas in epidermodysplasia verruciformis (EV) patients, are poorly understood. Using a yeast two-hybrid screening and molecular and cellular biology experiments, we found that HPV5 oncoprotein E6 interacts with SMAD3, a key component in the transforming growth factor beta 1 (TGF-beta 1) signaling pathway. HPV5 E6 inhibits SMAD3 transactivation by destabilizing the SMAD3/SMAD4 complex and inducing the degradation of both proteins. Interestingly, the E6 protein of nononcogenic EV HPV9 failed to interact with SMAD3, suggesting that downregulation of the TGF-beta 1 signaling pathway could be a determinant in HPV5 skin carcinogenesis.
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