Human papillomavirus (HPV) E6 interactions with Bak are conserved amongst E6 proteins from high and low risk HPV types.
Human papillomavirus (HPV) replication occurs in terminally differentiating epithelium, and requires the activation of cellular DNA replication proteins. Unscheduled DNA replication can result in the induction of apoptosis, and the viral E6 protein induces the degradation of p53 to prevent this. It has recently been shown that HPV-18 E6 can also stimulate the degradation of Bak, a pro-apoptotic member of the Bcl-2 family. This report shows that the E6 proteins from HPV-18, HPV-16 and HPV-11 can all bind to Bak in vitro, stimulate its degradation in vivo and reduce Bak-induced apoptosis. However, the non-oncogenic HPV-11 E6 is less effective than the oncogenic E6 proteins in each of these assays, indicating that the ability of HPV to circumvent the apoptosis induced by Bak may contribute to the oncogenic potential of the virus.
Thomas
M
M
Banks
L
L
D017209:Apoptosis; D015153:Blotting, Western; D002460:Cell Line; D004268:DNA-Binding Proteins; D005434:Flow Cytometry; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000378:metabolism*; D027383:Papillomaviridae / Q000235:genetics / Q000378:metabolism* / Q000472:pathogenicity*; D012097:Repressor Proteins; D014162:Transfection; D014779:Virus Replication; D050998:bcl-2 Homologous Antagonist-Killer Protein
C494772:BAK1 protein, human; D004268:DNA-Binding Proteins; C068651:E6 protein, Human papillomavirus type 16; C052603:E6 protein, Human papillomavirus type 18; D008565:Membrane Proteins; D009856:Oncogene Proteins, Viral; D012097:Repressor Proteins; D050998:bcl-2 Homologous Antagonist-Killer Protein