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Cancers 2014, 6(4), 1905-1924; doi:10.3390/cancers6041905

SUMO and KSHV Replication

1
Institute of Microbiology and Immunology, National Yang-Ming University, Taipei 112, Taiwan
2
Institute for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
3
Department of Biochemistry and Molecular Medicine, University of California, Davis, CA 95616, USA
4
UC Davis Cancer Center, University of California, Davis, CA 95616, USA
5
Division of Molecular and Genomic Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli County 35053, Taiwan
*
Author to whom correspondence should be addressed.
Received: 11 June 2014 / Revised: 9 September 2014 / Accepted: 10 September 2014 / Published: 29 September 2014
(This article belongs to the Special Issue DNA Viruses in Human Cancer)
View Full-Text   |   Download PDF [1019 KB, uploaded 29 September 2014]   |  

Abstract

Small Ubiquitin-related MOdifier (SUMO) modification was initially identified as a reversible post-translational modification that affects the regulation of diverse cellular processes, including signal transduction, protein trafficking, chromosome segregation, and DNA repair. Increasing evidence suggests that the SUMO system also plays an important role in regulating chromatin organization and transcription. It is thus not surprising that double-stranded DNA viruses, such as Kaposi’s sarcoma-associated herpesvirus (KSHV), have exploited SUMO modification as a means of modulating viral chromatin remodeling during the latent-lytic switch. In addition, SUMO regulation allows the disassembly and assembly of promyelocytic leukemia protein-nuclear bodies (PML-NBs), an intrinsic antiviral host defense, during the viral replication cycle. Overcoming PML-NB-mediated cellular intrinsic immunity is essential to allow the initial transcription and replication of the herpesvirus genome after de novo infection. As a consequence, KSHV has evolved a way as to produce multiple SUMO regulatory viral proteins to modulate the cellular SUMO environment in a dynamic way during its life cycle. Remarkably, KSHV encodes one gene product (K-bZIP) with SUMO-ligase activities and one gene product (K-Rta) that exhibits SUMO-targeting ubiquitin ligase (STUbL) activity. In addition, at least two viral products are sumoylated that have functional importance. Furthermore, sumoylation can be modulated by other viral gene products, such as the viral protein kinase Orf36. Interference with the sumoylation of specific viral targets represents a potential therapeutic strategy when treating KSHV, as well as other oncogenic herpesviruses. Here, we summarize the different ways KSHV exploits and manipulates the cellular SUMO system and explore the multi-faceted functions of SUMO during KSHV’s life cycle and pathogenesis. View Full-Text
Keywords: KSHV; SUMO; epigenetic; PML-NB; interferon KSHV; SUMO; epigenetic; PML-NB; interferon
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Chang, P.-C.; Kung, H.-J. SUMO and KSHV Replication. Cancers 2014, 6, 1905-1924.

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