Abstract
Cancer cells may undergo loss or alterations in functions that certain viruses normally target to promote virus replication. Virus mutants that have lost the targeting function(s) should be able to grow in such cancer cells but not in normal cells. A "tumor host range" (t-hr) selection procedure has been devised and applied to polyoma virus based on this rationale. Studies of one t-hr mutant have led to the identification of the mSal2 gene product (p150(sal2)) as a binding partner of the large T antigen. mSal2 encodes a multizinc finger protein and putative transcription factor homologous to the Drosophila homeotic gene Spalt. The t-hr mutant encodes an altered large T protein that fails to interact with p150(sal2) and is defective in replication and tumor induction in newborn mice.
Publication types
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Comparative Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3T3 Cells
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Amino Acid Sequence
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Animals
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Animals, Newborn
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Antigens, Polyomavirus Transforming / genetics*
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Base Sequence
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Carrier Proteins / genetics*
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Carrier Proteins / immunology*
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Cell Transformation, Viral / genetics
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DNA, Complementary / genetics
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DNA, Viral / genetics
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DNA-Binding Proteins
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Female
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Genes, Homeobox
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Genes, Insect
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Intracellular Signaling Peptides and Proteins*
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Male
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Mice
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Mice, Inbred C3H
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Molecular Sequence Data
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Mutation
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Polyomavirus / genetics*
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Polyomavirus / immunology*
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Polyomavirus / pathogenicity
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Polyomavirus Infections / etiology
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Sequence Deletion
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Transcription Factors
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Tumor Virus Infections / etiology
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Zinc Fingers / genetics
Substances
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Antigens, Polyomavirus Transforming
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Carrier Proteins
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DNA, Complementary
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DNA, Viral
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DNA-Binding Proteins
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Intracellular Signaling Peptides and Proteins
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Sall2 protein, mouse
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Transcription Factors