Insight into the function of the Golgi membrane protein GOLM1 in cholangiocytes through interactomic analysis

IF 3.5 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Meghana Nagaraj, Sharath Kumar Goud Emmagouni, Vaishali Chaurasiya, Luyang Li, Van Dien Nguyen, Salla Keskitalo, Markku Varjosalo, You Zhou, P. A. Nidhina Haridas, Vesa M. Olkkonen
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引用次数: 0

Abstract

GOLM1, a Golgi membrane protein, is upregulated in cancers and liver diseases. Analysis of public RNAseq data from healthy human liver suggested that GOLM1 is predominantly expressed in cholangiocytes. Therefore, this study was initiated to understand the molecular functions of GOLM1 in cholangiocytes through protein interactomics. The findings reveal a number of putative GOLM1-interacting partners involved in cellular regimes such as mitochondrial and Golgi functions, ribonucleoprotein biogenesis, cell cycle, and basement membrane organization. Further, to validate select key roles, GOLM1 was silenced in MMNK-1 cholangiocytes and the effects on cell functions were studied. The silencing resulted in impaired mitochondrial function, reduced mitochondrial and P-body markers, increased apoptosis, and reduced cell adhesion, suggesting crucial roles of GOLM1 in maintaining normal cholangiocyte metabolism and function.

Abstract Image

通过相互作用分析了解高尔基膜蛋白GOLM1在胆管细胞中的功能。
GOLM1是一种高尔基膜蛋白,在癌症和肝脏疾病中表达上调。对健康人肝脏公开RNAseq数据的分析表明,GOLM1主要在胆管细胞中表达。因此,本研究通过蛋白相互作用组学来了解GOLM1在胆管细胞中的分子功能。研究结果揭示了一些假定的golm1相互作用伙伴参与细胞机制,如线粒体和高尔基体功能、核糖核蛋白生物发生、细胞周期和基底膜组织。此外,为了验证所选择的关键作用,我们在MMNK-1胆管细胞中沉默GOLM1,并研究其对细胞功能的影响。沉默导致线粒体功能受损,线粒体和p体标记物减少,细胞凋亡增加,细胞粘附减少,提示GOLM1在维持正常胆管细胞代谢和功能方面发挥重要作用。
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来源期刊
FEBS Letters
FEBS Letters 生物-生化与分子生物学
CiteScore
7.00
自引率
2.90%
发文量
303
审稿时长
1.0 months
期刊介绍: FEBS Letters is one of the world''s leading journals in molecular biology and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, Research Letters and Hypotheses that merit urgent publication.
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