Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression

Proceedings of the National Academy of Sciences of the United States of America

Volumn 108, Issue 5, 2011, Pages 1919-1924

  Maruo, Seiji ^a   Zhao, Bo ^b   Johannsen, Eric ^b   Kieff, Elliott ^b   Zou, James ^b   Takada, Kenzo ^a  

^a HOKKAIDO UNIVERSITY   (Japan)

^b BRIGHAM AND WOMEN S HOSPITAL   (United States)

Author keywords

Cell cycle; CtBP; Lymphoma; Notch; Polycomb protein

Indexed keywords

CYCLIN DEPENDENT KINASE INHIBITOR 2A; EPSTEIN BARR VIRUS ANTIGEN; EPSTEIN BARR VIRUS ANTIGEN 3A; EPSTEIN BARR VIRUS ANTIGEN 3C; PROTEIN P53; UNCLASSIFIED DRUG;

ARTICLE; B LYMPHOCYTE; CELL GROWTH; CHROMATIN; CONTROLLED STUDY; CPG ISLAND; DNA METHYLATION; GENE INACTIVATION; GENE LOCUS; GENE REPRESSION; GENETIC TRANSCRIPTION; HISTONE MODIFICATION; HUMAN; HUMAN CELL; LYMPHOBLASTOID CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION;

CELL DIVISION; CELL LINE; CPG ISLANDS; CYCLIN-DEPENDENT KINASE INHIBITOR P16; DNA METHYLATION; EPSTEIN-BARR VIRUS NUCLEAR ANTIGENS; GENE KNOCKDOWN TECHNIQUES; HUMANS; PROMOTER REGIONS, GENETIC; TUMOR SUPPRESSOR PROTEIN P14ARF;

HUMAN HERPESVIRUS 4; HUMAN PAPILLOMAVIRUS;

EID: 79952170344     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1019599108     Document Type: Article

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