Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells

[1]  A. Ciechanover,et al.  Basal and human papillomavirus E6 oncoprotein-induced degradation of Myc proteins by the ubiquitin pathway. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[2]  G. Hannon,et al.  Myc activates telomerase. , 1998, Genes & development.

[3]  D. Wong,et al.  Inactivation of p16 in Human Mammary Epithelial Cells by CpG Island Methylation , 1998, Molecular and Cellular Biology.

[4]  C. Harley,et al.  Extension of life-span by introduction of telomerase into normal human cells. , 1998, Science.

[5]  Richard A. Ashmun,et al.  Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF , 1997, Cell.

[6]  M Fujita,et al.  Binding of high-risk human papillomavirus E6 oncoproteins to the human homologue of the Drosophila discs large tumor suppressor protein. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[7]  C B Harley,et al.  Telomerase catalytic subunit homologs from fission yeast and human. , 1997, Science.

[8]  R. Schlegel,et al.  The Human Papillomavirus Type 16 E6 and E7 Oncoproteins Dissociate Cellular Telomerase Activity from the Maintenance of Telomere Length* , 1997, The Journal of Biological Chemistry.

[9]  R. Haw,et al.  Evidence for the inactivation of multiple replicative lifespan genes in immortal human squamous cell carcinoma keratinocytes , 1997, Oncogene.

[10]  W. Klapper,et al.  Molecular basis of artifacts in the detection of telomerase activity and a modified primer for a more robust 'TRAP' assay. , 1997, Nucleic acids research.

[11]  G. Hannon,et al.  Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[12]  J. Nevins,et al.  Inhibition of cyclin D-CDK4/CDK6 activity is associated with an E2F-mediated induction of cyclin kinase inhibitor activity. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[13]  Galloway Da,et al.  HUMAN PAPILLOMAVIRUS TYPE 16 E7 ALLEVIATES A PROLIFERATION BLOCK IN EARLY PASSAGE HUMAN MAMMARY EPITHELIAL CELLS , 1996 .

[14]  J. McDougall,et al.  Telomerase activation by the E6 gene product of human papillomavirus type 16 , 1996, Nature.

[15]  E. Androphy,et al.  Mutational analysis of human papillomavirus type 16 E6 demonstrates that p53 degradation is necessary for immortalization of mammary epithelial cells , 1996, Journal of virology.

[16]  J. Shay,et al.  Modifications of a telomeric repeat amplification protocol (TRAP) result in increased reliability, linearity and sensitivity. , 1995, Nucleic acids research.

[17]  C B Harley,et al.  Specific association of human telomerase activity with immortal cells and cancer. , 1994, Science.

[18]  G. Demers,et al.  Growth arrest by induction of p53 in DNA damaged keratinocytes is bypassed by human papillomavirus 16 E7. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[19]  S. Barber,et al.  Restoration of telomeres in human papillomavirus-immortalized human anogenital epithelial cells , 1994, Molecular and cellular biology.

[20]  J. Shay,et al.  The frequency of immortalization of human fibroblasts and mammary epithelial cells transfected with SV40 large T-antigen. , 1993, Experimental cell research.

[21]  M. Scheffner,et al.  Cloning and expression of the cDNA for E6-AP, a protein that mediates the interaction of the human papillomavirus E6 oncoprotein with p53 , 1993, Molecular and cellular biology.

[22]  C B Harley,et al.  Telomere length predicts replicative capacity of human fibroblasts. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[23]  J. Shay,et al.  The two-stage mechanism controlling cellular senescence and immortalization , 1992, Experimental Gerontology.

[24]  G. Demers,et al.  The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells , 1991, Journal of virology.

[25]  Arnold J. Levine,et al.  The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53 , 1990, Cell.

[26]  D. Lowy,et al.  HPV16 E6 and E7 proteins cooperate to immortalize human foreskin keratinocytes. , 1989, The EMBO journal.

[27]  R. Schlegel,et al.  The E6 and E7 genes of the human papillomavirus type 16 together are necessary and sufficient for transformation of primary human keratinocytes , 1989, Journal of virology.

[28]  L. Hayflick.  THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS. , 1965, Experimental cell research.

[29]  J. Shay,et al.  E6 of human papillomavirus type 16 can overcome the M1 stage of immortalization in human mammary epithelial cells but not in human fibroblasts. , 1993, Oncogene.

[30]  V. Band,et al.  Human papilloma virus DNAs immortalize normal human mammary epithelial cells and reduce their growth factor requirements. , 1990, Proceedings of the National Academy of Sciences of the United States of America.