The Early HPV16 Proteins Can Regulate mRNA Levels of Cell Cycle Genes in Human Cervical Carcinoma Cells by p53-Independent Mechanisms

This publication has 57 references indexed in Scilit:

• HPV16 E6 Oncoprotein Stimulates the Transforming Growth Factor-β1 Promoter in Fibroblasts through a Specific GC-Rich Sequence
  Virology, 1997
• p53-dependent and -independent transactivation by the E6 protein of human papillomavirus type 16
  Journal of General Virology, 1996
• Interaction of Papillomavirus E6 Oncoproteins with a Putative Calcium-Binding Protein
  Science, 1995
• The E6 Protein of Human Papillomavirus Type 16 Functions as a Transcriptional Repressor in a Mechanism Independent of the Tumor Suppressor Protein, p53
  Virology, 1994
• Growth arrest by induction of p53 in DNA damaged keratinocytes is bypassed by human papillomavirus 16 E7.
  Proceedings of the National Academy of Sciences, 1994
• Wild-type p53 can down-modulate the activity of various promoters.
  Proceedings of the National Academy of Sciences, 1991
• Constitutive expression of c-myc oncogene confers hormone independence and enhanced growth-factor responsiveness on cells transformed by human papilloma virus type 16.
  Proceedings of the National Academy of Sciences, 1989
• Differential Effect of Platelet-derived Growth Factor- Versus Serum-induced Growth on Smooth Muscle α-Actin and Nonmuscle β-Actin mRNA Expression in Cultured Rat Aortic Smooth Muscle Cells
  Journal of Biological Chemistry, 1989
• The Human Papilloma Virus-16 E7 Oncoprotein Is Able to Bind to the Retinoblastoma Gene Product
  Science, 1989
• Analysis of the structure and expression of the c-myc oncogene in cervical tumor and in cervical tumor-derived cell lines
  Biochemical and Biophysical Research Communications, 1989