期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 57, 期 3, 页码 F35-F39出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-16-0106
关键词
store-operated Ca2+ entry; TRPC1; STIM1; Orai1; insulin secretion; pancreatic beta-cells
资金
- Swiss National Science Foundation [31003A-155897]
- Agence Nationale de la Recherche [ANR-15-CE14-0005]
- Swiss National Science Foundation (SNF) [31003A_155897] Funding Source: Swiss National Science Foundation (SNF)
Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic beta-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (K-ATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels ( VDCC). The subsequent rapid rise in cytoplasmic free Ca2+ concentration triggers insulin exocytosis. However, despite more than 40 years of investigation, certain aspects of the intracellular Ca2+ responses to glucose and secretagogues remain unexplained, suggesting the involvement of additional Ca2+ channels. Here, we discuss the emerging role of store-operated Ca2+ channels carried by Orai1 and transient receptor potential canonical 1 (TRPC1) proteins and regulated by the stromal interaction molecule 1 (STIM1) in the control of glucose-induced insulin secretion. The role of other voltage-independent cation channels formed by other members of the TRP channels family is also addressed.
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