期刊
MICROORGANISMS
卷 9, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/microorganisms9040685
关键词
Marek’ s disease virus; US3; protein kinase; PML; SP100
类别
资金
- Texas AM University
The study reveals that MDV US3 disrupts PML and SP100 in a kinase dependent manner, and a proteasome dependent degradation pathway is involved in this disruption process. These findings provide the first evidence for the interplay between MDV proteins and PML-NBs.
Promyelocytic leukemia protein nuclear bodies (PML-NBs) are dynamic nuclear structures, shown to be important for herpesvirus replication; however, their role in regulating Marek's disease virus (MDV) infection has not been studied. MDV is an oncogenic alphaherpesvirus that causes lymphoproliferative disease in chickens. MDV encodes a US3 serine/threonine protein kinase that is important for MDV replication and gene expression. In this study, we studied the role of MDV US3 in regulating PML-NBs. Using an immunofluorescence assay, we found that MDV US3 disrupts PML and SP100 in a kinase dependent manner. In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100. These findings provide the first evidence for the interplay between MDV proteins and PML-NBs.
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