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通过ST3GAL3介导的LDLR选择性α2,3-化促进了囊泡性口腔炎病毒的进入

Tomoya Isaji¹, Feng Qi², Yu-Chun Chien³

¹Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai, Miyagi 981-8558, Japan.

Biochimica et biophysica acta. General subjects

|February 24, 2026

概括

主体细胞化,特别是由ST3GAL3,对于膀性口炎病毒 (VSV) 通过LDLR受体有效进入至关重要. 这一途径对于VSV-G依赖性感染至关重要,并可能为瘤性VSV策略提供点.

科学领域:

病毒学病毒学
葡萄糖生物学葡萄糖生物学
细胞生物学细胞生物学

背景情况:

膀性口腔炎病毒 (VSV) 的感染性取决于其糖蛋白 (VSV-G).
低密度脂蛋白受体 (LDLR) 是VSV-G的主要受体.
宿主化在VSV入侵中的作用尚不清楚.

研究的目的:

调查宿主化在VSV-G依赖病毒入口中的作用.
为了确定基转移酶ST3GAL3,ST3GAL4或ST3GAL6是否参与VSV的进入.
分析化对VSV感染中LDLR功能的影响.

主要方法:

产生了缺乏ST3GAL3,ST3GAL4或ST3GAL6.6的HeLa细胞系.
使用流细胞计和显微镜评估病毒关联,吸收和转导.
使用莱克结合和LC-MS/MS糖蛋白组学分析了LDLR化.

主要成果:

淘汰ST3GAL3显著降低了VSV的关联,吸收和转导.
在ST3GAL3缺乏下降了LDLR N-甘氨酸的α2,3-连接化.
ST3GAL3的重新表达恢复了病毒的进入,其他基转移酶没有补偿.

结论:

对于高效的VSV输入来说,对LDLRN-糖的ST3GAL3依赖性化是必不可少的.
因此,ST3GAL4和ST3GAL6不能补偿HeLa细胞中ST3GAL3的损失.
确定了对VSV-G感染至关重要的特定的糖化途径,突出了ST3GAL3作为调节病毒热带和性VSV策略的潜在目标.

关键词:

葡萄糖基酶化是指葡萄糖基酶化.低密度脂蛋白受体 (LDLR) 是一种基转移酶是一种基转移酶.病毒感染病毒感染.这是一种α2,3-化.

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