Bird G S, Louzao M C, Ribeiro C M, Putney J W
Calcium Regulation Section, Lab. Signal Transduction, Nat. Inst. Environmental Health Sciences, NIH Research Triangle Park, NC 27709, USA.
Eur J Morphol. 1998 Aug;36 Suppl:153-6.
In exocrine gland cells, stimulation of a variety of surface receptors initiates a Ca2+ signalling system through activation of a polyphosphoinositide-specific phospholipase C. One product of phospholipase C activity, inositol 1,4,5-trisphosphate ((1,4,5)IP3), signals the release of intracellular Ca2+. Release of intracellular Ca2+ is followed by entry of Ca2+ into the cell across the plasma membrane. The mechanism by which Ca2+ entry is regulated is not well understood, although it is clear that (1,4,5)IP3 plays an important role. One hypothesis suggests that Ca2+ entry is triggered by the depletion of intracellular Ca2+ stores by (1,4,5)IP3, a process termed 'capacitative calcium entry'. The purpose of these studies is to gain understanding into the processes controlling capacitative calcium entry in exocrine gland cells.
在外分泌腺细胞中，多种表面受体的刺激通过激活多磷酸肌醇特异性磷脂酶C启动Ca2+信号系统。磷脂酶C活性的一个产物，肌醇1,4,5-三磷酸（(1,4,5)IP3），发出细胞内Ca2+释放的信号。细胞内Ca2+释放后，Ca2+通过质膜进入细胞。虽然很明显(1,4,5)IP3起着重要作用，但Ca2+进入的调节机制尚不清楚。一种假说认为，Ca2+进入是由(1,4,5)IP3导致细胞内Ca2+储存耗尽所触发的，这一过程称为“容量性钙内流”。这些研究的目的是深入了解控制外分泌腺细胞容量性钙内流的过程。
