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PMID: 3016992 Published · ppublish English Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

An SV40 mutant T antigen does not bind the SV40 viral origin.

Virology ·Vol. 153 ·No. 2 ·1986-09-00 ·Pages 297-309

Sompayrac L, Danna KJ

Abstract

F8dl is an SV40 deletion mutant that lacks over 60% of the coding sequences for large T antigen and yet is able to immortalize early passage rat cells, to transform established cell lines, and to cause tumors in animals. We report here on the further characterization of this mutant and show that (a) transformation by F8dl is protein mediated but does not require the action of the SV40 small t antigen; (b) the F8dl T antigens have, or are associated with, an ATPase activity; (c) the 34-kDa mutant T antigen of F8dl is localized in nuclei and cell membranes of F8dl transformants and binds to double-stranded DNA; (d) the 20-25 kDa forms of the mutant T antigen are cytoplasmic; and (e) the F8dl T antigens do not bind with high affinity to the SV40 origin of viral DNA replication.

MeSH Terms
Adenosine Triphosphatases/analysis Animals Antigens, Polyomavirus Transforming Antigens, Viral, Tumor/analysis,genetics,physiology Cell Transformation, Neoplastic DNA/metabolism DNA Replication DNA, Viral/analysis,metabolism Fluorescent Antibody Technique Mice Mutation Oncogene Proteins, Viral/analysis,genetics,physiology Simian virus 40/genetics,immunology,pathogenicity Virus Replication
Chemicals
Antigens, Polyomavirus Transforming Antigens, Viral, Tumor DNA, Viral Oncogene Proteins, Viral DNA Adenosine Triphosphatases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Sompayrac L
Danna K J
Article Info
Journal
Virology
Abbr.
Virology
ISSN
0042-6822
Published
1986-09-00
Pages
297-309
Language
English
Region
United States
NLM ID
0110674
Subset
IM
Grants
NCI NIH HHS · CA-34072 · United States
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