Type-specific interaction between human papillomavirus type 58 E2 protein and E7 protein inhibits E7-mediated oncogenicity.
Human papillomavirus type 58 (HPV-58) is a very common HPV type in eastern Asia. Little is known about its biology and tumorigenesis. In this study, HPV-58 E2 protein (58E2) was found to interact with E7 protein (58E7), and the hinge domain of 58E2 was shown to be responsible for binding ... to the 58E7 protein. Interestingly, the E2-E7 interaction appears to be HPV type-specific, as we found that the HPV-16 E2 could not bind to the 58E7 protein, and neither did 58E2 interact with HPV-16 E7. The biological consequence(s) of the E2-E7 interaction in HPV-58, especially in viral tumorigenesis, was investigated. Results showed that, through interacting with 58E7, 58E2 prevented E7-induced retinoblastoma protein (pRb) degradation and prolonged the half-life of pRb in cells. Additionally, 58E2 abrogated 58E7-induced cell proliferation. These observations collectively suggest that direct interaction with 58E7 is another mechanism for 58E2 to inhibit 58E7-associated carcinogenesis in addition to regulating expression of the 58E7 gene.
Mesh Terms:
Asia, Cell Proliferation, Cell Transformation, Viral, Cells, Cultured, Humans, Oncogene Proteins, Viral, Papillomaviridae, Protein Binding, Protein Interaction Mapping, Retinoblastoma Protein, Viral Envelope Proteins
Asia, Cell Proliferation, Cell Transformation, Viral, Cells, Cultured, Humans, Oncogene Proteins, Viral, Papillomaviridae, Protein Binding, Protein Interaction Mapping, Retinoblastoma Protein, Viral Envelope Proteins
J Gen Virol
Date: Jul. 01, 2012
PubMed ID: 22442110
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