使用基于turboid的接近标记技术的中间电导钙依赖性钾通道（KCa3.1）相互作用蛋白：对胰腺肿瘤相互作用组和相关信号通路的见解

IF 4 2区生物学 Q2 CELL BIOLOGY

Journal of Cellular Physiology Pub Date : 2025-09-15 DOI:10.1002/jcp.70092

Veronica Carpanese, Soha Sadeghi, Luca Matteo Todesca, Ildikò Szabò, Vanessa Checchetto

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引用次数: 0

摘要

KCa3.1离子通道是一种钙活化的钾离子通道，表达于多种组织中，表现为质膜和线粒体的双重定位。该通道在许多癌症中高度表达，并与增殖和迁移的调节有关。然而，与KCa3.1在癌细胞中发挥的调节作用相关的信号通路的分子细节尚未完全阐明。因此，我们在完整的KPC胰腺癌细胞中使用接近标记确定了KCa3.1的相互作用组，这反映了人类胰腺癌的侵袭性转移行为。结果强调了一些新的相互作用，包括那些驻留在细胞膜内。根据我们目前对KCa3.1和胰腺癌的了解，我们讨论了KCa3.1通道邻近体和相关途径，这些信息可在公共数据库中获得。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Intermediate Conductance Calcium-Dependent Potassium Channel (KCa3.1) Interacting Proteins Using Turboid-Based Proximity Labeling Technology: Insights Into Interactome and Related Signaling Pathways in Pancreatic Tumors

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K_Ca3.1 ion channel is a calcium-activated potassium channel expressed in various tissues, showing dual localization to the plasma membrane and to mitochondria. This channel is highly expressed in numerous cancers and has been implicated in the regulation of proliferation and migration. The molecular details of the signaling pathways linked to regulation exerted by K_Ca3.1 in cancer cells are, however, not fully elucidated yet. Therefore, we determined the interactome of K_Ca3.1 using proximity labeling in intact KPC pancreatic cancer cells that mirror the aggressive metastatic behavior of human pancreatic cancer. The results highlight several novel interactors, including those residing in intracellular membranes. The K_Ca3.1 channel proxisome and related pathways are discussed in light of our current knowledge about K_Ca3.1 and pancreatic cancer, available in public databases.

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来源期刊

Journal of Cellular Physiology 生物-生理学

CiteScore

14.70

自引率

0.00%

发文量

256

审稿时长

1 months

期刊介绍： The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.