Journal article
Roles for herpes simplex virus type 1 UL34 and US3 proteins in disrupting the nuclear lamina during herpes simplex virus type 1 egress
Virology (New York, N.Y.), Vol.347(2), pp.261-276
04/10/2006
DOI: 10.1016/j.virol.2005.11.053
PMCID: PMC2993110
PMID: 16427676
Abstract
Cells infected with wild type HSV-1 showed significant lamin A/C and lamin B rearrangement, while U
L
34-null virus-infected cells exhibited few changes in lamin localization, indicating that U
L
34 is necessary for lamin disruption. During HSV infection, U
S
3 limited the development of disruptions in the lamina, since cells infected with a U
S
3-null virus developed large perforations in the lamin layer. U
S
3 regulation of lamin disruption does not correlate with the induction of apoptosis. Expression of either U
L
34 or U
S
3 proteins alone disrupted lamin A/C and lamin B localization. Expression of U
L
34 and U
S
3 together had little effect on lamin A/C localization, suggesting a regulatory interaction between the two proteins. The data presented in this paper argue for crucial roles for both U
L
34 and U
S
3 in regulating the state of the nuclear lamina during viral infection.
Details
- Title: Subtitle
- Roles for herpes simplex virus type 1 UL34 and US3 proteins in disrupting the nuclear lamina during herpes simplex virus type 1 egress
- Creators
- Susan L BjerkeRichard J Roller
- Resource Type
- Journal article
- Publication Details
- Virology (New York, N.Y.), Vol.347(2), pp.261-276
- DOI
- 10.1016/j.virol.2005.11.053
- PMID
- 16427676
- PMCID
- PMC2993110
- NLM abbreviation
- Virology
- ISSN
- 0042-6822
- eISSN
- 1096-0341
- Language
- English
- Date published
- 04/10/2006
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984001129602771
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