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IRGB10 寡聚化的结构基础由 GTP 水解介导。

Structural basis of IRGB10 oligomerization by GTP hydrolysis.

机构信息

College of Pharmacy, Chung-Ang University, Seoul, Republic of Korea.

Department of Global Innovative Drugs, Graduate School of Chung-Ang University, Seoul, Republic of Korea.

出版信息

Front Immunol. 2023 Aug 29;14:1254415. doi: 10.3389/fimmu.2023.1254415. eCollection 2023.

Abstract

Immunity-related GTPase B10 (IRGB10) is a crucial member of the interferon (IFN)-inducible GTPases and plays a vital role in host defense mechanisms. Following infection, IRGB10 is induced by IFNs and functions by liberating pathogenic ligands to activate the inflammasome through direct disruption of the pathogen membrane. Despite extensive investigation into the significance of the cell-autonomous immune response, the precise molecular mechanism underlying IRGB10-mediated microbial membrane disruption remains elusive. Herein, we present two structures of different forms of IRGB10, the nucleotide-free and GppNHp-bound forms. Based on these structures, we identified that IRGB10 exists as a monomer in nucleotide-free and GTP binding states. Additionally, we identified that GTP hydrolysis is critical for dimer formation and further oligomerization of IRGB10. Building upon these observations, we propose a mechanistic model to elucidate the working mechanism of IRGB10 during pathogen membrane disruption.

摘要

免疫相关鸟苷三磷酸酶 B10(IRGB10)是干扰素(IFN)诱导的鸟苷三磷酸酶家族的重要成员,在宿主防御机制中发挥着至关重要的作用。在感染后,IRGB10 被 IFNs 诱导,并通过直接破坏病原体膜来释放致病配体激活炎症小体来发挥作用。尽管人们对细胞自主免疫反应的重要性进行了广泛的研究,但 IRGB10 介导的微生物膜破坏的确切分子机制仍不清楚。在此,我们展示了两种不同形式的 IRGB10 的结构,即无核苷酸和 GppNHp 结合形式。基于这些结构,我们确定 IRGB10 在无核苷酸和 GTP 结合状态下以单体形式存在。此外,我们还确定了 GTP 水解对于 IRGB10 二聚体形成以及进一步寡聚化是至关重要的。基于这些观察结果,我们提出了一个机制模型,以阐明 IRGB10 在破坏病原体膜过程中的工作机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4026/10495984/def2193417c2/fimmu-14-1254415-g001.jpg

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