IgSF11-PKM2通路对破骨细胞基因表达的影响。

microPublication biology Pub Date : 2025-03-24 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001469
Hyunsoo Kim, Noriko Takegahara, Yongwon Choi
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引用次数: 0

摘要

破骨细胞是原发性骨吸收细胞。之前,我们通过igsf11介导的糖酵解酶PKM2的磷酸化描述了破骨细胞的代谢调节。在这里,我们报告了IgSF11-PKM2介导的调节对破骨细胞基因表达的影响,利用RNA测序对破骨细胞进行了改造,以表达缺乏IgSF11的嵌合蛋白,并从药理学上调节PKM2活性。我们的分析确定了破骨细胞相关基因,其表达因缺乏IgSF11和PKM2活性的变化而改变。本研究揭示了与IgSF11-PKM2通路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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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.

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