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Updated: Jun 29, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

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DNA聚合酶的祖先等位基因改变了抗病毒耐受性

Yilin Kang1, Jussi Hepojoki2,3, Rocio Sartori Maldonado1

  • 1Stem Cell and Metabolism Research Program Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland.

Nature
|April 3, 2024
PubMed
概括

线粒体DNA聚合酶 (POLG1) 缺陷会损害抗病毒防御,导致线粒体疾病的变异性. 这种p.W748S变种破坏了线粒体DNA的稳定性,导致免疫缺陷和神经和肝脏问题.

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Translesion DNA Polymerases

Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
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