Human embryonic kidney cells: stable transformation with an origin-defective simian virus 40 DNA and use as hosts for human papovavirus replication.
AUTOR(ES)
Major, E O
RESUMO
An origin-defective mutant DNA of simian virus 40 immortalized human embryonic kidney cells, maintaining a T protein which could function for human papovavirus BK DNA replication but not for human papovavirus JC DNA replication. Neither BK virions nor capsid proteins were produced in these cells. This may indicate that the simian virus 40 T protein in human embryonic kidney cells is competent for maintaining transformation and initiating and completing DNA replication for BK but is not competent for switching to late gene functions. Furthermore, it appears that the JC DNA replication origin cannot efficiently use the simian virus 40 T protein for its DNA synthesis, as suggested by its DNA sequence data (R. Frisque, J. Virol. 46:170-176, 1983; T. Miyamura, H. Jikoya, E. Soeda, and K. Yoshiike, J. Virol. 45:73-79, 1983).
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=368707Documentos Relacionados
- Characterization of human tracheal epithelial cells transformed by an origin-defective simian virus 40.
- Immortalization of human fibroblasts transformed by origin-defective simian virus 40.
- Expression of early genes of origin-defective mutants of simian virus 40.
- Simian virus 40-transformed human cells that express large T antigens defective for viral DNA replication.
- Extended life span of human endometrial stromal cells transfected with cloned origin-defective, temperature-sensitive simian virus 40.