Ambudkar Indu S
Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
Sci STKE. 2004 Jul 20;2004(243):pe32. doi: 10.1126/stke.2432004pe32.
Stimulation of cell surface receptors that increase phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis leads to intracellular Ca2+ release and activation of plasma membrane Ca2+ entry channels. Ca2+ entry via these channels regulates a wide array of physiological functions. The molecular composition of these channels and the mechanisms that activate or inactivate them have not yet been elucidated. Members of the TRPC subfamily of the TRP (transient receptor potential) family of proteins have been recently suggested as molecular components of these channels. In addition, Ca2+ signaling proteins and the signals they generate are compartmentalized and spatiotemporally regulated. Thus, the mechanisms involved in the assembly and trafficking of Ca2+ signaling proteins, including TRPC channels, will determine the regulation of Ca2+ entry and its effect on cellular function.
刺激增加磷脂酰肌醇4,5 - 二磷酸（PIP2）水解的细胞表面受体，会导致细胞内Ca2+释放并激活质膜Ca2+进入通道。通过这些通道的Ca2+进入调节着广泛的生理功能。这些通道的分子组成以及激活或使其失活的机制尚未阐明。TRP（瞬时受体电位）蛋白家族的TRPC亚家族成员最近被认为是这些通道的分子组成部分。此外，Ca2+信号蛋白及其产生的信号是被分隔且受到时空调节的。因此，参与包括TRPC通道在内的Ca2+信号蛋白组装和运输的机制，将决定Ca2+进入的调节及其对细胞功能的影响。
