Abstract
Vectors carrying the origin of replication (oriP) and driving expression of the EBNA-1 protein from Epstein-Barr virus (EBV) replicate as extrachromosomal episomes in human cells. Whether these vectors can be maintained as episomes in murine cells is still controversial. Here we demonstrate that EBNA-1 expression alone was unable to maintain episomal expression of an EBV-based vector in the murine Sp2/0 cell line. However, we were able to obtain long-term episome maintenance in Sp2/0 cells after exogenously expressing human EBP2 by genetic engineering. Our results provide further evidence for the fundamental role of human EBP2 in episomal maintenance of EBV-based vectors. Moreover, we demonstrate that EBV-based vectors can be successfully used in cells presumably incompetent for episomal maintenance.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Carrier Proteins / genetics*
-
Carrier Proteins / metabolism
-
Cell Line, Tumor
-
DNA Replication / genetics*
-
Epstein-Barr Virus Nuclear Antigens / genetics*
-
Epstein-Barr Virus Nuclear Antigens / metabolism
-
Gene Expression
-
Genetic Vectors / genetics
-
Herpesvirus 4, Human / genetics*
-
Herpesvirus 4, Human / metabolism
-
Humans
-
Intracellular Signaling Peptides and Proteins
-
Mice
-
Multiple Myeloma / genetics*
-
Multiple Myeloma / metabolism
-
Plasmids / genetics*
-
Plasmids / metabolism
-
Protein Binding / genetics
-
RNA-Binding Proteins
-
Replication Origin / genetics*
Substances
-
Carrier Proteins
-
EBNA1BP2 protein, human
-
Ebna1bp2 protein, mouse
-
Epstein-Barr Virus Nuclear Antigens
-
Intracellular Signaling Peptides and Proteins
-
RNA-Binding Proteins
-
EBV-encoded nuclear antigen 1