JC virus T' proteins encoded by alternatively spliced early mRNAs enhance T antigen-mediated viral DNA replication in human cells

2001 ◽  
Vol 7 (3) ◽  
pp. 250-264 ◽  
Author(s):  
Cindy Prins, Richard J Frisque
PLoS ONE ◽  
2010 ◽  
Vol 5 (5) ◽  
pp. e10606 ◽  
Author(s):  
Brigitte Bollag ◽  
Catherine A. Hofstetter ◽  
Marta M. Reviriego-Mendoza ◽  
Richard J. Frisque

1983 ◽  
Vol 3 (9) ◽  
pp. 1670-1674
Author(s):  
W J Muller ◽  
M A Naujokas ◽  
J A Hassell

The frequency of transformation of rodent fibroblasts by polyomavirus is enhanced by a viral gene product, large T-antigen. However, this effect of large T-antigen cannot be demonstrated with pBR322-cloned viral DNA. Recently, it was discovered that pBR322 contains cis-acting sequences inhibitory to DNA replication in mammalian cells. Because polyomavirus large T-antigen is required for viral DNA replication, we examined the possibility that our inability to demonstrate a requirement for large T-antigen in transformation with pBR322-cloned viral DNA was due to the failure of the chimeric DNA to replicate in the transfected cells. To this end we constructed polyomavirus recombinant molecules with a plasmid (pML-2) that lacks these "poison" sequences and measured their capacity to transform cells. Here we report that recombinant plasmids capable of replicating in the transfected cells transform these cells at frequencies approximately sixfold greater than their replication-defective counterparts.


1997 ◽  
Vol 11 (9) ◽  
pp. 1098-1110 ◽  
Author(s):  
K S Campbell ◽  
K P Mullane ◽  
I A Aksoy ◽  
H Stubdal ◽  
J Zalvide ◽  
...  

1983 ◽  
Vol 3 (9) ◽  
pp. 1670-1674 ◽  
Author(s):  
W J Muller ◽  
M A Naujokas ◽  
J A Hassell

The frequency of transformation of rodent fibroblasts by polyomavirus is enhanced by a viral gene product, large T-antigen. However, this effect of large T-antigen cannot be demonstrated with pBR322-cloned viral DNA. Recently, it was discovered that pBR322 contains cis-acting sequences inhibitory to DNA replication in mammalian cells. Because polyomavirus large T-antigen is required for viral DNA replication, we examined the possibility that our inability to demonstrate a requirement for large T-antigen in transformation with pBR322-cloned viral DNA was due to the failure of the chimeric DNA to replicate in the transfected cells. To this end we constructed polyomavirus recombinant molecules with a plasmid (pML-2) that lacks these "poison" sequences and measured their capacity to transform cells. Here we report that recombinant plasmids capable of replicating in the transfected cells transform these cells at frequencies approximately sixfold greater than their replication-defective counterparts.


1990 ◽  
Vol 64 (12) ◽  
pp. 6234-6245 ◽  
Author(s):  
I Reynisdóttir ◽  
D R O'Reilly ◽  
L K Miller ◽  
C Prives

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