Epstein-Barr virus nuclear antigen-1 colocalizes with lamin B1 in the nucleoplasm and along the nuclear rim

Epstein-Barr virus nuclear antigen-1 colocalizes with lamin B1 in the nucleoplasm and along the... Epstein-Barr virus nuclear antigen 1 (EBNA-1) is essential for the maintenance of latent EBV plasmids, and is also a transcriptional regulator. Nuclear lamins, components of the nuclear lamina, have also been found in the nucleoplasm. We report here that EBNA-1 coincided with lamin B1 in the nucleoplasm and around the nuclear rim during S-phase by confocal microscopy of cells transfected with EBNA-1 in the absence of EBV plasmids. Lamin B1, which is rarely detected in nuclear soluble fractions, was detected in chromatin and nuclear matrix fractions of the EBNA-1-expressing cells. These observations suggest that EBNA-1 colocalizes with lamin B1 in the subnuclear sites. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Epstein-Barr virus nuclear antigen-1 colocalizes with lamin B1 in the nucleoplasm and along the nuclear rim

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Publisher
Springer Journals
Copyright
Copyright © 2003 by Springer-Verlag/Wien
Subject
LifeSciences
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-003-0122-9
Publisher site
See Article on Publisher Site

Abstract

Epstein-Barr virus nuclear antigen 1 (EBNA-1) is essential for the maintenance of latent EBV plasmids, and is also a transcriptional regulator. Nuclear lamins, components of the nuclear lamina, have also been found in the nucleoplasm. We report here that EBNA-1 coincided with lamin B1 in the nucleoplasm and around the nuclear rim during S-phase by confocal microscopy of cells transfected with EBNA-1 in the absence of EBV plasmids. Lamin B1, which is rarely detected in nuclear soluble fractions, was detected in chromatin and nuclear matrix fractions of the EBNA-1-expressing cells. These observations suggest that EBNA-1 colocalizes with lamin B1 in the subnuclear sites.

Journal

Archives of VirologySpringer Journals

Published: Aug 1, 2003

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