Functions of herpesvirus-encoded homologs of the cellular ribonucleotide reductase large subunitFunctions of Herpesvirus-Encoded Homologs of the Cellular Ribonucleotide Reductase Large Subunit
- Other Titles
- Functions of Herpesvirus-Encoded Homologs of the Cellular Ribonucleotide Reductase Large Subunit
- Authors
- Kwon, K.M.[Kwon, K.M.]; Ahn, J.-H.[Ahn, J.-H.]
- Issue Date
- 2016
- Publisher
- Chonnam National University Medical School
- Keywords
- Herpesvirus; Immune signaling; Ribonucleotide reductase large subunit
- Citation
- Journal of Bacteriology and Virology, v.46, no.4, pp.326 - 329
- Indexed
- SCOPUS
KCI
- Journal Title
- Journal of Bacteriology and Virology
- Volume
- 46
- Number
- 4
- Start Page
- 326
- End Page
- 329
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/40097
- DOI
- 10.4167/jbv.2016.46.4.326
- ISSN
- 1598-2467
- Abstract
- Deoxyribonucleotides (dNTPs) are important for the efficient growth of DNA viruses. Therefore, many DNA viruses have strategies for the upregulation of cellular dNTP levels. Both α- and γ-herpesviruses encode functional homologs of cellular dNTP anabolic enzymes, including the class I ribonucleotide reductase (RNR) large (R1) and small (R2) subunits, whereas β-herpesviruses modulate host cells to induce genes that increase dNTP levels. Interestingly, β-herpesviruses still express the nonfunctional RNR R1 subunit. However, it is not clear why β-herpesviruses still carry inactive R1 homologs. Recently, the R1 homologs of herpesviruses have been shown to inhibit innate immune signaling pathways. In particular, both functional and nonfunctional R1 homologs target receptor-interacting protein kinase 1 (RIP1) and inhibit RIP1-mediated signaling pathways to promote viral replication. Here, we summarize recent findings on the activity of herpesviral R1 homologs and discuss their roles in the regulation of innate immune signaling pathways. © 2016, Chonnam National University Medical School. All rights reserved.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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