甲状旁腺激素
内科学
内分泌学
甲状旁腺主细胞
钙
信使核糖核酸
钙代谢
化学
甲状旁腺激素受体
细胞外
分泌物
基因表达
生物
钙敏感受体
基因
生物化学
激素受体
医学
癌症
乳腺癌
出处
期刊:Endocrinology
[Oxford University Press]
日期:2009-12-23
卷期号:151 (4): 1398-1402
被引量:31
摘要
PTH regulates serum calcium and phosphate levels and bone strength. The parathyroid is unique in that the trigger for PTH secretion is a low extracellular calcium rather than high calcium as for other hormones. The parathyroid senses small changes in serum calcium through the seven-trans-membrane G protein-coupled calcium receptor to alter PTH secretion. PTH then acts on bone and kidney to correct serum calcium. Parathyroid cells have few secretory granules as compared with other endocrine cells, and therefore PTH production is regulated largely at the levels of PTH gene expression and parathyroid cell proliferation. The regulation of PTH gene expression by changes in calcium and phosphate and in chronic kidney failure is posttranscriptional involving the binding of trans-acting proteins to a defined cis element in the PTH mRNA 3′-untranslated region. These protein-PTH mRNA interactions are orchestrated by the peptidyl-prolyl isomerase Pin1. This review discusses the mechanisms of regulation of PTH mRNA stability determining serum PTH levels and mineral metabolism.
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