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Publications by E Espling
Abrogation of Growth Arrest Signals by Human Papillomavirus Type 16 E7 Is Mediated by Sequences Required for Transformation.
Journal of Virology
Insect Science
Immunology
Microbiology
Virology
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Destabilization of the Retinoblastoma Tumor Suppressor by Human Papillomavirus Type 16 E7 Is Not Sufficient to Overcome Cell Cycle Arrest in Human Keratinocytes
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Human Papillomavirus Type 16 E7 Oncoprotein mediatesCCNA1promoter Methylation
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Human Papillomavirus Type 16 Nucleoprotein E7 Is a Tumor Rejection Antigen.
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Regulation of the Cdc25A Gene by the Human Papillomavirus Type 16 E7 Oncogene
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Negative Charge at the Casein Kinase II Phosphorylation Site Is Important for Transformation but Not for Rb Protein Binding by the E7 Protein of Human Papillomavirus Type 16.
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Human Papillomavirus Type 16 E7 Maintains Elevated Levels of the Cdc25A Tyrosine Phosphatase During Deregulation of Cell Cycle Arrest
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The E7 Protein of Human Papillomavirus Type 16 Sensitizes Primary Human Keratinocytes to Apoptosis
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Human Papillomavirus Type 16 E7 Oncoprotein Binds and Inactivates Growth-Inhibitory Insulin-Like Growth Factor Binding Protein 3
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