Departments of Medicine, Hematology/Oncology and Pharmacology, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States.
Cell Calcium. 2011 Sep;50(3):234-41. doi: 10.1016/j.ceca.2011.05.011. Epub 2011 May 31.
The Bcl-2 protein, best known for its ability to inhibit apoptosis, interacts with the inositol 1,4,5-trisphosphate receptor (IP(3)R) Ca(2+) channel to regulate IP(3)-mediated Ca(2+) release from the endoplasmic reticulum. This review summarizes the current state of knowledge regarding the interaction of Bcl-2, and also its homologue Bcl-xl, with the IP(3)R and how these interactions regulate Ca(2+) signaling. The dual role of these interactions in promoting prosurvival Ca(2+) signals, while at the same time inhibiting proapoptotic Ca(2+) signals, is discussed. Moreover, this review will elucidate the recently recognized importance of the Bcl-2-IP(3)R interaction in human disease.
Bcl-2 蛋白以其抑制细胞凋亡的能力而闻名,它与肌醇 1,4,5-三磷酸受体 (IP(3)R) Ca(2+)通道相互作用,以调节内质网中由 IP(3)介导的 Ca(2+)释放。本综述总结了关于 Bcl-2 及其同源物 Bcl-xl 与 IP(3)R 相互作用以及这些相互作用如何调节 Ca(2+)信号的最新知识。讨论了这些相互作用在促进促生存 Ca(2+)信号的同时抑制促凋亡 Ca(2+)信号的双重作用。此外,本综述还阐明了 Bcl-2-IP(3)R 相互作用在人类疾病中的重要性。