Zhang Chen, Miller Cassandra Lynn, Brown Edward M, Yang Jenny J
Department of Chemistry, Georgia State University, Atlanta, Georgia, 30303, USA.
Sci China Life Sci. 2015 Jan;58(1):14-27. doi: 10.1007/s11427-014-4779-y. Epub 2015 Jan 10.
The Ca(2+)-sensing receptor (the CaSR), a G-protein-coupled receptor, regulates Ca(2+) homeostasis in the body by monitoring extracellular levels of Ca(2+) ([Ca(2+)]o) and responding to a diverse array of stimuli. Mutations in the Ca(2+)-sensing receptor result in hypercalcemic or hypocalcemic disorders, such as familial hypocalciuric hypercalcemia, neonatal severe primary hyperparathyroidism, and autosomal dominant hypocalcemic hypercalciuria. Compelling evidence suggests that the CaSR plays multiple roles extending well beyond not only regulating the level of extracellular Ca(2+) in the human body, but also controlling a diverse range of biological processes. In this review, we focus on the structural biology of the CaSR, the ligand interaction sites as well as their relevance to the disease associated mutations. This systematic summary will provide a comprehensive exploration of how the CaSR integrates extracellular Ca(2+) into intracellular Ca(2+) signaling.
钙敏感受体(CaSR)是一种G蛋白偶联受体,通过监测细胞外钙离子水平([Ca(2+)]o)并对多种刺激做出反应来调节体内的钙稳态。钙敏感受体的突变会导致高钙血症或低钙血症疾病,如家族性低钙血症性高钙血症、新生儿重症原发性甲状旁腺功能亢进症和常染色体显性遗传性低钙血症性高钙尿症。有力证据表明,CaSR发挥的多种作用不仅远远超出了调节人体细胞外钙离子水平的范畴,还涉及控制一系列不同的生物学过程。在本综述中,我们聚焦于CaSR的结构生物学、配体相互作用位点及其与疾病相关突变的关联性。这一系统总结将全面探讨CaSR如何将细胞外钙离子整合到细胞内钙离子信号传导中。