Abstract：
Ca2+ plays a crucial role in cell signaling, cytosolic Ca2+ can change up to 10,000-fold in concentration due to the action of Ca2+-ATPases, including PMCA, SERCA and SCR. The regulation and balance of these enzymes are essential to maintain cytosolic Ca2+ homeostasis. Our laboratory has discovered a novel PMCA regulatory system, involving acetylated tubulin alone or in combination with membrane lipids. This regulation controls cytosolic Ca2+ levels and influences cellular properties such as erythrocyte rheology. This review summarizes the findings on the regulatory mechanism of PMCA activity by acetylated tubulin in combination with lipids. The combination of tubulin cytoskeleton and membrane lipids suggests a novel regulatory system for PMCA, which consequently affects cytosolic Ca2+ content, depending on cytoskeletal and plasma membrane dynamics. Understanding the interaction between acetylated tubulin, lipids and PMCA activity provides new insights into Ca2+ signaling and cell function. Further research may shed light on potential therapeutic targets for diseases related to Ca2+ dysregulation. This discovery contributes to a broader understanding of cellular processes and offers opportunities to develop innovative approaches to treat Ca2+-related disorders. By elucidating the complex regulatory mechanisms of Ca2+ homeostasis, we advance our understanding of cell biology and its implications for human health.
摘要：
Ca2+在细胞信号传导中起着至关重要的作用，由于Ca2+-ATPases的作用，胞质Ca2+的浓度可以改变高达10,000倍，包括PMCA,SERCA和SCR。这些酶的调节和平衡是维持细胞溶质Ca2+稳态所必需的。我们的实验室发现了一种新的PMCA监管系统，涉及乙酰化微管蛋白单独或与膜脂质组合。这种调节控制胞质Ca2+水平并影响细胞特性如红细胞流变学。本文总结了乙酰化微管蛋白与脂质联合对PMCA活性调节机制的发现。微管蛋白细胞骨架和膜脂质的结合表明了一种新的PMCA调节系统，从而影响细胞溶质Ca2+含量，取决于细胞骨架和质膜动力学。了解乙酰化微管蛋白之间的相互作用，脂质和PMCA活性为Ca2+信号和细胞功能提供了新的见解。进一步的研究可能会揭示与Ca2调节异常相关的疾病的潜在治疗靶标。这一发现有助于更广泛地理解细胞过程，并为开发治疗Ca2相关疾病的创新方法提供了机会。通过阐明Ca2+稳态的复杂调节机制,我们推进了对细胞生物学及其对人类健康的影响的理解。
