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PMID: 1850016 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Mutual functional antagonism of the simian virus 40 T antigen and the hepatitis B virus trans activator.

Journal of virology ·Vol. 65 ·No. 5 ·1991-05-00 ·Pages 2351-6

Seto E, Yen TS

Abstract

The hepatitis B virus X protein (pX) trans activates transcription of a wide variety of viral and cellular genes, apparently by interacting with multiple cellular transcription factors. It has been shown previously that the simian virus 40 early-region gene products (large-T and small-t antigens) prevent trans activation by pX. We show here that this phenomenon can be ascribed solely to the large-T antigen and that T antigen binds to pX in vitro. Mapping studies reveal that the region of large-T antigen around residues 125 and 126 is critical for this binding and also for the ability of T antigen to prevent trans activation by pX. Furthermore, pX in turn interferes with two of the known functions of T antigen, transcriptional trans activation and simian virus 40 DNA replication. We propose that pX and T antigen inactivate each other by forming a nonfunctional complex in vivo.

MeSH Terms
Animals Antigens, Polyomavirus Transforming/antagonists & inhibitors,metabolism Cells, Cultured Hepatitis B Antigens/antagonists & inhibitors,metabolism Mutation Plasmids Precipitin Tests Simian virus 40/immunology Trans-Activators/antagonists & inhibitors,metabolism Transcriptional Activation Transfection Viral Regulatory and Accessory Proteins
Chemicals
Antigens, Polyomavirus Transforming Hepatitis B Antigens Trans-Activators Viral Regulatory and Accessory Proteins hepatitis B virus X protein
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Seto E
Department of Pathology, Veterans Affairs Medical Center, San Francisco, California.
Yen T S
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1991-05-00
Pages
2351-6
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC240586
Subset
IM
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