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免疫球蛋白超家族成员11-丙酮酸激酶M2通路对破骨细胞基因表达的影响。

The impact of IgSF11-PKM2 pathway on gene expression in osteoclasts.

作者信息

Kim Hyunsoo, Takegahara Noriko, Choi Yongwon

机构信息

Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.

出版信息

MicroPubl Biol. 2025 Mar 24;2025. doi: 10.17912/micropub.biology.001469. eCollection 2025.

DOI:10.17912/micropub.biology.001469
PMID:40196137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11973584/
Abstract

Osteoclasts are primary bone resorbing cells. Previously, we described metabolic regulation of osteoclasts through IgSF11-mediated phosphorylation of the glycolytic enzyme PKM2. Here, we report the impact of IgSF11-PKM2-mediated regulation on gene expression in osteoclasts, utilizing RNA sequencing on osteoclasts engineered to express a chimeric protein, lacking IgSF11, and pharmacologically modulating PKM2 activity. Our analysis identified osteoclast-related genes whose expression is altered by the absence of IgSF11 and by changes in PKM2 activity. This study reveals gene expression changes associated with the IgSF11-PKM2 pathway, providing new insight into its role in osteoclasts.

摘要

破骨细胞是主要的骨吸收细胞。此前,我们描述了通过免疫球蛋白超家族成员11(IgSF11)介导的糖酵解酶丙酮酸激酶M2(PKM2)磷酸化对破骨细胞的代谢调节。在此,我们利用对经基因工程改造以表达缺乏IgSF11的嵌合蛋白的破骨细胞进行RNA测序,并通过药理学方法调节PKM2活性,报告了IgSF11 - PKM2介导的调节对破骨细胞基因表达的影响。我们的分析确定了与破骨细胞相关的基因,其表达因IgSF11的缺失和PKM2活性的变化而改变。这项研究揭示了与IgSF11 - PKM2途径相关的基因表达变化,为其在破骨细胞中的作用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e95/11973584/293cb90efebf/25789430-2025-micropub.biology.001469.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e95/11973584/293cb90efebf/25789430-2025-micropub.biology.001469.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e95/11973584/293cb90efebf/25789430-2025-micropub.biology.001469.jpg

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Nrf2 differentially regulates osteoclast and osteoblast differentiation for bone homeostasis.Nrf2通过差异调节破骨细胞和成骨细胞分化来维持骨稳态。
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Bone Res. 2023 Mar 16;11(1):17. doi: 10.1038/s41413-023-00251-2.
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FSTL1 promotes liver fibrosis by reprogramming macrophage function through modulating the intracellular function of PKM2.FSTL1 通过调节 PKM2 的细胞内功能重编程巨噬细胞功能促进肝纤维化。
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J Cell Sci. 2020 May 27;133(10):jcs239772. doi: 10.1242/jcs.239772.
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