This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Edbauer, C Articles by Williams, J Search for Related Content PubMed PubMed Citation Articles by Edbauer, C Articles by Williams, J

 Previous Article  |  Next Article 

J Virol. 1988 September; 62(9): 3265-3273

Adenovirus type 12 E1B 19-kilodalton protein is not required for oncogenic transformation in rats.

Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213-3890.

ABSTRACT

The adenovirus type 12 mutants in700 and pm700 carry site-specific mutations within the reading frame encoding the E1B 19-kilodalton protein (19K protein) which prevent the production of the intact 19K protein. In cultures of human A549 cells, these mutants grow just as well as the wild-type virus does, but they display a large-plaque (lp), cytocidal (cyt) phenotype. DNA in these infected cells is not degraded, but at late times in human KB cells infected by the mutants, the mutants display a DNA degradation (deg) phenotype. The transformation phenotype of these mutants is also host range. Although the mutants are defective for transformation of the 3Y1 rat cell line, they transform rat and mouse primary kidney cells in vitro at wild-type efficiency and are capable of inducing tumors in rats. These results support the view that the type 12 E1B 19K protein is not obligatory for oncogenic transformation.

This article has been cited by other articles:

• Turnell, A. S., Grand, R. J. A., Gallimore, P. H. (1999). The Replicative Capacities of Large E1B-Null Group A and Group C Adenoviruses Are Independent of Host Cell p53 Status. J. Virol. 73: 2074-2083 [Abstract] [Full Text]