期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 113, 期 8, 页码 2229-2234出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1525444113
关键词
EBNA1; RPL4; NCL; EBV; oriP
资金
- National Science Council [NSC 101-2320-B320-005-MY3]
- Ministry of Science and Technology [MOST 104-2320-B-320-013]
- National Health Research Institutes [NHRI-EX-1025-9910BC, NHRI-EX103-10307BI]
- National Institutes of Health [5R01CA047006, 5R01CA085180, 5R01CA170023]
Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1)-mediated origin of plasmid replication (oriP) DNA episome maintenance is essential for EBV-mediated tumorigenesis. We have now found that EBNA1 binds to Ribosome Protein L4 (RPL4). RPL4 shRNA knockdown decreased EBNA1 activation of an oriP luciferase reporter, EBNA1 DNA binding in lymphoblastoid cell lines, and EBV genome number per lymphoblastoid cell line. EBV infection increased RPL4 expression and redistributed RPL4 to cell nuclei. RPL4 and Nucleolin (NCL) were a scaffold for an EBNA1-induced oriP complex. The RPL4 N terminus cooperated with NCL-K429 to support EBNA1 and oriP-mediated episome binding and maintenance, whereas the NCL C-terminal K380 and K393 induced oriP DNA H3K4me2 modification and promoted EBNA1 activation of oriP-dependent transcription. These observations provide new insights into the mechanisms by which EBV uses NCL and RPL4 to establish persistent B-lymphoblastoid cell infection.
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