D Liebowitz
Harvard University
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Featured researches published by D Liebowitz.
Molecular and Cellular Biology | 1987
D Liebowitz; R Kopan; E Fuchs; Jeffery T. Sample; Elliott Kieff
The Epstein-Barr virus (EBV) latent infection membrane protein (LMP) is likely to be an important mediator of EBV-induced cell proliferation, since it is one of the few proteins encoded by the virus in latent infection and since production of this protein in Rat-1 cells results in their conversion to a fully transformed phenotype. LMP was previously noted to localize to patches at the cell periphery. In this paper we examine the basis of LMP patching in EBV-infected, transformed lymphocytes. Our data indicate that LMP is associated with the cytoskeletal protein vimentin. Although LMP is fully soluble in isotonic Triton X-100 buffer, only 50% of it is extracted from cells in this solution. The rest remains bound to the cytoskeleton. LMP undergoes phosphorylation, and phosphorylated LMP is preferentially associated with the cytoskeleton. As judged by both immunofluorescence and immunoelectron microscopy, the vimentin network in EBV-transformed lymphocytes or EBV-infected Burkitt tumor lymphocytes is abnormal. Vimentin and LMP often colocalize in a single patch near the plasma membrane. In response to Colcemid treatment of EBV-infected cells, vimentin reorganizes into perinuclear rings, as it does in uninfected cells. LMP is associated with these perinuclear rings. Vimentin (or a vimentin-associated protein) may be a transducer of an LMP transmembrane effect in lymphoproliferation.
Archive | 1989
D Liebowitz; Elliott Kieff; Jeffery T. Sample; Mark Birkenbach; Fred Wang
Primary Epstein-Barr Virus (EBV) infection begins in the oropharynx where the virus establishes persistent infection of epithelial cells through continued cycles of infection, virus replication, cell death, virus release and infection of new cells. Early in primary infection, virus spreads from epithelial cells to subepithelial B lymphocytes. Infected B lymphocytes are largely non-permissive for virus replication. EBV establishes latent infection in B lymphocytes and transforms these cells so that they can secrete immunoglobulin and proliferate indefinitely in vitro. In immune deficient humans, EBV infected lymphocytes can also proliferate into malignant tumors. In latently infected B lymphocytes, EBV characteristically expresses a restricted set of virus genes which are presumed to i) maintain latent virus genome persistence, ii) cause the B lymphocyte growth transformation associated with latent viral infection and iii) represent targets for the immune response which is responsible for the prevention of outgrowth of latently infected B lymphocytes in humans.
Journal of Virology | 1990
F Wang; Christopher D. Gregory; Clare E. Sample; Meredith L. Rowe; D Liebowitz; R J Murray; Alan B. Rickinson; Elliott Kieff
Journal of Virology | 1988
D Wang; D Liebowitz; F Wang; Christopher D. Gregory; Alan B. Rickinson; Richard S. Larson; Timothy A. Springer; Elliott Kieff
Journal of Virology | 1986
D Liebowitz; D Wang; Elliott Kieff
Journal of Virology | 1989
Jeffery T. Sample; D Liebowitz; Elliott Kieff
Journal of Virology | 1988
D Wang; D Liebowitz; Elliott Kieff
Journal of Virology | 1992
D Liebowitz; John A. Mannick; Kenzo Takada; Elliott Kieff
Journal of Virology | 1989
Mark Birkenbach; D Liebowitz; F Wang; Jeffery T. Sample; Elliott Kieff
Journal of Virology | 1989
D Liebowitz; Elliott Kieff