Evidence for gene silencing by DNA methylation in normal human diploid fibroblasts

1995 ◽  
Vol 21 (3) ◽  
pp. 215-218 ◽  
Author(s):  
Robin Holliday ◽  
Thu Ho
Keyword(s):  
Dna Methylation ◽  
Gene Silencing ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Normal Human

scholarly journals Reversible cellular senescence: implications for immortalization of normal human diploid fibroblasts.

1989 ◽  
Vol 9 (7) ◽  
pp. 3088-3092 ◽  
Author(s):  
W E Wright ◽  
O M Pereira-Smith ◽  
J W Shay
Keyword(s):  
Cellular Senescence ◽  
Rare Event ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Normal Human ◽  
Immortal Cells ◽  
Cellular Dna

IMR-90 normal human diploid fibroblasts, transfected with a steroid inducible mouse mammary tumor virus-driven simian virus 40 T antigen, were carried through crisis to yield an immortal cell line. Growth was dependent on the presence of the inducer (dexamethasone) during both the extended precrisis life span of the cells and after immortalization. After dexamethasone removal, immortal cells divided once or twice and then accumulated in G1. These results are best explained by a two-stage model for cellular senescence. Mortality stage 1 (M1) causes a loss of mitogen responsiveness and arrest near the G1/S interface and can be bypassed or overcome by the cellular DNA synthesis-stimulating activity of T antigen. Mortality stage 2 (M2) is an independent mechanism that is responsible for the failure of cell division during crisis. The inactivation of M2 is a rare event, probably of mutational origin in human cells, independent of or only indirectly related to the expression of T antigen. Under this hypothesis, T-antigen-immortalized cells contain an active but bypassed M1 mechanism and an inactivated M2 mechanism. These cells are dependent on the continued expression of T antigen for the maintenance of immortality for the same reason that precrisis cells are dependent on T antigen for growth: both contain an active M1 mechanism.

scholarly journals Molecular pathways executing the “trophic sentinel” response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation

Virology ◽  
2004 ◽  
Vol 319 (1) ◽  
pp. 81-93 ◽  
Author(s):  
Alexandra Eichten ◽  
Debrah S Rud ◽  
Miranda Grace ◽  
Siribang-on Piboonniyom ◽  
Valerie Zacny ◽  
...  
Keyword(s):  
Growth Factor ◽  
Molecular Pathways ◽  
Hpv 16 ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Growth Factor Deprivation ◽  
Normal Human
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