The human papillomavirus type 16 E6 oncogene induces premature mitotic chromosome segregation.
Expression of the human papillomavirus type 16 E6 and E7 oncogenes initiates and maintains abnormal cell replication, by interacting with the p53 and retinoblastoma (Rb) gene products. Subsequent changes in host cell gene expression, as a consequence of genetic instability, can result in progression to invasive carcinoma. In addition to previously described effects of these viral oncogenes on centrosome synthesis, primarily associated with the expression of E7, the results described herein demonstrate that the E6 oncogene can induce premature chromosome segregation in human cells.
Plug-Demaggio
Annemieke W
AW
Department of Pathology, University of Washington, 1959 Pacific Street, N.E., Seattle, Washington, WA 98195-7407, USA.
McDougall
James K
JK
D015153:Blotting, Western; D002478:Cells, Cultured; D002875:Chromosomes; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D015603:Keratinocytes / Q000166:cytology; D008938:Mitosis / Q000235:genetics*; D009856:Oncogene Proteins, Viral / Q000235:genetics*; D009857:Oncogenes; D012097:Repressor Proteins
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D012097:Repressor Proteins