BIOMAT Database Logo BIOMAT Database Logo

Potential cellular functions of Epstein-Barr Nuclear Antigen 1 (EBNA1) of Epstein-Barr Virus. 2013

Danielle Westhoff Smith, and Bill Sugden
Department of Oncology, McArdle Laboratory for Cancer Research, Madison, WI 53706, USA. dwesthoff@wisc.edu

Epstein-Barr Nuclear Antigen 1 (EBNA1) is a multifunctional protein encoded by EBV. EBNA1's role in maintaining EBV in latently proliferating cells, by mediating EBV genome synthesis and nonrandom partitioning to daughter cells, as well as regulating viral gene transcription, is well characterized. Less understood are the roles of EBNA1 in affecting the host cell to provide selective advantages to those cells that harbor EBV. In this review we will focus on the interactions between EBNA1 and the host cell that may provide EBV-infected cells selective advantages beyond the maintenance of EBV.

UI MeSH Term Description Entries
D004854 Herpesvirus 4, Human The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies. Burkitt Herpesvirus,Burkitt Lymphoma Virus,E-B Virus,EBV,Epstein-Barr Virus,Human Herpesvirus 4,Infectious Mononucleosis Virus,Burkitt's Lymphoma Virus,HHV-4,Herpesvirus 4 (gamma), Human,Burkitts Lymphoma Virus,E B Virus,E-B Viruses,Epstein Barr Virus,Herpesvirus, Burkitt,Infectious Mononucleosis Viruses,Lymphoma Virus, Burkitt,Mononucleosis Virus, Infectious,Mononucleosis Viruses, Infectious
D005786 Gene Expression Regulation Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation. Gene Action Regulation,Regulation of Gene Expression,Expression Regulation, Gene,Regulation, Gene Action,Regulation, Gene Expression
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D054884 Host-Pathogen Interactions The interactions between a host and a pathogen, usually resulting in disease. Host Pathogen Interaction,Host-Pathogen Relations,Pathogen-Host Interaction,Pathogen-Host Interactions,Host Pathogen Interactions,Host Pathogen Relations,Host-Pathogen Interaction,Host-Pathogen Relation,Interaction, Host Pathogen,Interaction, Host-Pathogen,Interaction, Pathogen-Host,Interactions, Host Pathogen,Interactions, Host-Pathogen,Interactions, Pathogen-Host,Pathogen Host Interaction,Pathogen Host Interactions,Pathogen Interaction, Host,Pathogen Interactions, Host,Relation, Host-Pathogen,Relations, Host-Pathogen
D019309 Epstein-Barr Virus Nuclear Antigens Nuclear antigens encoded by VIRAL GENES found in HUMAN HERPESVIRUS 4. At least six nuclear antigens have been identified. EBV Nuclear Antigen,EBV Nuclear Antigens,Epstein-Barr Virus Nuclear Antigen,Herpesvirus 4, Human Nuclear Antigens,Nuclear Antigens, Herpesvirus 4, Human,Antigen, EBV Nuclear,Epstein Barr Virus Nuclear Antigen,Epstein Barr Virus Nuclear Antigens,Nuclear Antigen, EBV,Nuclear Antigens, EBV
D020031 Epstein-Barr Virus Infections Infection with human herpesvirus 4 (HERPESVIRUS 4, HUMAN); which may facilitate the development of various lymphoproliferative disorders. These include BURKITT LYMPHOMA (African type), INFECTIOUS MONONUCLEOSIS, and oral hairy leukoplakia (LEUKOPLAKIA, HAIRY). EBV Infections,Epstein-Barr Virus Infection,Herpesvirus 4 Infections, Human,Human Herpes Virus 4 Infections,Human Herpesvirus 4 Infections,Infections, EBV,Infections, Epstein-Barr Virus,EBV Infection,Epstein Barr Virus Infection,Epstein Barr Virus Infections,Infection, EBV,Infection, Epstein-Barr Virus,Virus Infection, Epstein-Barr,Virus Infections, Epstein-Barr

Related Publications

Danielle Westhoff Smith, and Bill Sugden
A potential NES of the Epstein-Barr virus nuclear antigen 1 (EBNA1) does not confer shuttling.
March 1999, FEBS letters,
Danielle Westhoff Smith, and Bill Sugden
Lymphomas driven by Epstein-Barr virus nuclear antigen-1 (EBNA1) are dependant upon Mdm2.
July 2018, Oncogene,
Danielle Westhoff Smith, and Bill Sugden
Epstein-Barr virus nuclear antigen 1 (EBNA1) induced cytotoxicity in epithelial cells is associated with EBNA1 degradation and processing.
September 2003, Virology,
Danielle Westhoff Smith, and Bill Sugden
Requirements for Epstein-Barr nuclear antigen 1 (EBNA1)-induced permanganate sensitivity of the epstein-barr virus latent origin of DNA replication.
October 1997, The Journal of biological chemistry,
Danielle Westhoff Smith, and Bill Sugden
Genome-wide analysis of host-chromosome binding sites for Epstein-Barr Virus Nuclear Antigen 1 (EBNA1).
October 2010, Virology journal,
Danielle Westhoff Smith, and Bill Sugden
Contributions of Epstein-Barr nuclear antigen 1 (EBNA1) to cell immortalization and survival.
September 2012, Viruses,
Danielle Westhoff Smith, and Bill Sugden
Identification of Potential Inhibitors against Epstein-Barr Virus Nuclear Antigen 1 (EBNA1): An Insight from Docking and Molecular Dynamic Simulations.
August 2021, ACS chemical neuroscience,
Danielle Westhoff Smith, and Bill Sugden
Mitotic chromosome interactions of Epstein-Barr nuclear antigen 1 (EBNA1) and human EBNA1-binding protein 2 (EBP2).
December 2009, Journal of cell science,
Danielle Westhoff Smith, and Bill Sugden
Epstein-Barr virus nuclear antigen 1 (EBNA1) protein induction of epithelial-mesenchymal transition in nasopharyngeal carcinoma cells.
February 2014, Cancer,
Danielle Westhoff Smith, and Bill Sugden
Epstein-barr-virus nuclear antigen.
January 1982, Progress in medical virology. Fortschritte der medizinischen Virusforschung. Progres en virologie medicale,
Copied contents to your clipboard!