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PMID: 6316342 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

A frameshift mutation affecting the carboxyl terminus of the simian virus 40 large tumor antigen results in a replication- and transformation-defective virus.

Lewis ED, Chen S, Kumar A, Blanck G, Pollack RE, Manley JL

Abstract

We have constructed a frameshift mutation in the simian virus 40 early region using a novel method of oligonucleotide-directed mutagenesis. The mutated DNA specifies an 84,000-dalton large tumor antigen that consists of approximately equal to 75,000 daltons encoded by the wild-type reading frame and 9,000 daltons, by the alternative reading frame (wild-type large tumor antigen is approximately equal to 82,000 daltons). The frameshifted carboxyl terminus of the protein bears a strong similarity to the same region of polyoma virus middle-sized tumor antigen. We have found that the mutant DNA is unable to replicate when introduced into permissive monkey cells and incapable of transforming nonpermissive mouse cells.

MeSH Terms
Amino Acid Sequence Animals Antigens, Viral, Tumor/genetics Base Sequence Cell Line Cell Transformation, Viral Chlorocebus aethiops DNA Replication DNA Restriction Enzymes Kidney Molecular Weight Mutation Plasmids Simian virus 40/genetics,immunology Transfection Virus Replication
Chemicals
Antigens, Viral, Tumor DNA Restriction Enzymes
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Lewis E D
Chen S
Kumar A
Blanck G
Pollack R E
Manley J L
References (33)
33 references, click to expand
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1983-12-00
Pages
7065-9
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC389993
Subset
IM
Grants
NCI NIH HHS · CA 25066 · United States
NCI NIH HHS · CA33620 · United States
NIGMS NIH HHS · GM 28983 · United States
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