Expression of 100,000-M(r) simian virus 40 (SV40) tumor antigen in mouse fibroblasts transfected with replication-defective SV40 genomes

Michael Verderame, R. Pollack

Research output: Contribution to journalArticle

Abstract

Simian virus 40 early region mutants which are partially or completely replication defective were tested for their ability to transform postcrisis mouse fibroblasts. All mutants tested were capable of generating anchorage-independent transformants. We have previously reported the presence of a variant tumor antigen of 100,000 M(r) (100K protein) generated upon transformation by wild-type simian virus 40 virions which correlates with anchorage-independent growth. In this study, none of the mutants tested produced the 100K variant protein at early (before the fifth) passage. Long-term passage (>20 weeks) permitted the expression of this 100K variant in half of the transformants. Thus the phenotype of these mutants is different from both wild-type simian virus 40 (frequently production of 100K by the third passage, and always by the tenth passage) and the origin-minus class of mutants (no production of 100K at any passage).

Original languageEnglish (US)
Pages (from-to)857-863
Number of pages7
JournalJournal of Virology
Volume57
Issue number3
StatePublished - Jan 1 1986

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Simian virus 40
Defective Viruses
Neoplasm Antigens
fibroblasts
Fibroblasts
Genome
antigens
mutants
neoplasms
genome
mice
Virion
Proteins
Phenotype
virion
Growth
proteins
phenotype

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

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abstract = "Simian virus 40 early region mutants which are partially or completely replication defective were tested for their ability to transform postcrisis mouse fibroblasts. All mutants tested were capable of generating anchorage-independent transformants. We have previously reported the presence of a variant tumor antigen of 100,000 M(r) (100K protein) generated upon transformation by wild-type simian virus 40 virions which correlates with anchorage-independent growth. In this study, none of the mutants tested produced the 100K variant protein at early (before the fifth) passage. Long-term passage (>20 weeks) permitted the expression of this 100K variant in half of the transformants. Thus the phenotype of these mutants is different from both wild-type simian virus 40 (frequently production of 100K by the third passage, and always by the tenth passage) and the origin-minus class of mutants (no production of 100K at any passage).",
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