Randriamampita C, Tsien R Y
Department of Pharmacology, University of California, San Diego, La Jolla 92093-0647.
Nature. 1993 Aug 26;364(6440):809-14. doi: 10.1038/364809a0.
Intracellular Ca2+ signals that last more than a few minutes after the onset of stimulation depend critically on influx of extracellular Ca2+. Such Ca2+ influx can be triggered in many cell types by depletion of intracellular Ca2+ stores without detectable elevations of known messengers. The mechanism by which store depletion can control plasma membrane Ca2+ permeability remains controversial. Here we present evidence for a novel soluble mediator. Calcium depletion of a lymphocyte cell line caused the messenger to be released from intracellular organelles into the cytoplasm and to a much lesser extent into the extracellular medium. The messenger caused Ca2+ influx when applied to macrophages, astrocytoma cells, and fibroblasts and was therefore named CIF (for Ca(2+)-influx factor). CIF appears to have hydroxyls (or hydroxyl and amino groups) on adjacent carbons, a phosphate, and a M(r) under 500.
刺激开始后持续数分钟以上的细胞内钙离子信号严重依赖于细胞外钙离子的内流。在许多细胞类型中，细胞内钙离子储存的耗尽可触发这种钙离子内流，而此时已知信使分子却未出现可检测到的升高。储存耗尽控制质膜钙离子通透性的机制仍存在争议。在此，我们提供了一种新型可溶性介质的证据。淋巴细胞系的钙离子耗尽导致该信使分子从细胞内细胞器释放到细胞质中，释放到细胞外介质中的程度则小得多。将该信使分子应用于巨噬细胞、星形细胞瘤细胞和成纤维细胞时会引起钙离子内流，因此被命名为CIF（钙离子内流因子）。CIF似乎在相邻碳原子上有羟基（或羟基和氨基）、一个磷酸基团，且相对分子质量低于500。
