作者: L. Szekely , G. Selivanova , K. P. Magnusson , G. Klein , K. G. Wiman
关键词: Molecular biology 、 Virology 、 Retinoblastoma 、 Nuclear protein 、 Epstein–Barr virus 、 Biology 、 Binding site 、 Point mutation 、 Retinoblastoma protein 、 DNA-binding protein 、 Tumor suppressor gene
摘要: Abstract Epstein-Barr virus (EBV) immortalized human lymphoblastoid cell lines express six virally encoded nuclear proteins, designated EBV antigens 1-6 (EBNA-1-6). We show that the EBNA-5 protein (alternatively EBNA-LP) is required for B-cell transformation can form a molecular complex with retinoblastoma (RB) and p53 tumor suppressor proteins. Using deletion mutants, we have found 66-amino acid-long peptide, by W repeat of genome, sufficient binding. Point mutations RB inhibit their complexing other DNA viral oncoproteins do not affect binding to EBNA-5. competes Our data suggest mechanisms involved in may include impairment function.