基础研究

PARP10 相变凝聚通过改写 NAD⁺ 稳态抑制病毒复制

来源:Nat Commun · PMID 42934229 · DOI 10.1038/s41467-026-78058-y** · 来源:IMA 知识库《文献层·文献监控卡片》2026-10-29 期 · 全文级(file_id dGBunAeRiRlm,下载实测 692,872 B) · 全文已获取并通过归属校验

数据日期 2026-10-29 · 生成时间 2026-10-29 06:03

研究问题

Despite growing interest, the extent to which phase separation regulates enzymatic activity and the functional consequences of elevated activity within condensates remain poorly understood.

方法

Bone-marrow-derived macrophages (BMDMs) were isolated from the tibia and femur of C57BL/6 mice.;[Mouse models] All mice were on C57BL/6 background.;Parp10-/-, Parp103E/3E, Parp10G837W/G837W and mEGFP-Parp10 knock-in (Parp10mEGFP/mEGFP) mice were generated via CRISPR/Cas9 mediated gene editing by Cyagen Bioscience Inc.;Mice were maintained under specific-pathogen-free conditions with controlled temperature (18–23 °C), humidity (40–60%) and a 12-h light/12-h dark cycle.

核心结论

Statistical significance levels are denoted as follows: *p < 0.05 and p < 0.01.;Biological n = 3. j Normalized VSV mRNA levels in BHK-21 cells transfected with GFP or GFP-PARP10 and infected with VSV (8 hpi, MOI = 1.5).;Biological n = 3. l Normalized VSV mRNA levels in negative control (sgRNA targeting lacZ) or MAVS knockout (KO) HEK293T cells transfected with GFP vector or GFP-PARP10 and infected with VSV (8 hpi, MOI = 1.5). ‖ 结论**:Our study revealed the biochemical basis for PARP10 condensation and suggested a potentially broader regulatory principle for the compartmentalization of other ARTD enzymes.

局限

Therefore, more physiological stimuli to induce PARP10 condensation in vitro warrant further investigation.;Future studies will determine whether PARP10 directly binds and modifies viral components, and how such modifications influence virion assembly.;Although we have excluded the possibility that PARP10 exerts antiviral effects via regulation of the type I interferon pathway, we cannot rule out the possibility that PARP10 modifies other host proteins to affect innate immune responses.

对本项目的价值

★★★★★ NAD⁺ 轴是最接近临床可转化的代谢干预节点,直接影响 NAD 前体 / CD38 抑制策略取舍。顶刊证据;命中核心 NAD⁺轴;最大样本量约 299;设计 单细胞。

全文来源

PMC JATS 全文(正文 110,785 字符,已过标题/DOI 逐字归属校验)

原文题录

  • 英文标题:PARP10 condensation inhibits viral replication via targeting NAD+ homeostasis.
  • 期刊与标识:Nat Commun · PMID 42934229 · DOI 10.1038/s41467-026-78058-y**

B 级证据分级:B 级(同行评议临床前研究,主要为动物模型)

本文核心结论来自动物模型或体外细胞学,属临床前证据,不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义,与人类临床结局之间仍有距离。

关于本文的文献来源:本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写,依据已获取的期刊全文(方法、样本量与结论已回到原文核对);未能获取全文的同批条目另行标注「摘要级」,全程未做任何数值推算补全。