Kiselyov Kirill, Kim Joo Young, Zeng Weizhong, Muallem Shmuel
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Pflugers Arch. 2005 Oct;451(1):116-24. doi: 10.1007/s00424-005-1442-2. Epub 2005 Jul 26.
Since their identification in the concluding years of the last century, the mammalian transient receptor potential (canonical) (TRPC) channels have remained in the limelight as the primary candidates for the Ca(2+) entry pathway activated by the hormones, growth factors, and neurotransmitters that exert their effect through activation of PLC. Although TRPC channels have been shown clearly to mediate, at least in part, receptor-activated Ca(2+) entry in literally all cell types, several of their central characteristics, as recorded in expression systems using recombinant channels, differ from those of the native receptor-dependent Ca(2+) influx channels. The present review attempts to highlight the interaction of TRPC channels with other proteins, which may explain the variability of TRPC channel activation and regulatory mechanisms observed with the native and recombinant channels. These include the homologous and heterotopous interactions of TRPC channel isoforms, the interaction of TRPC channels with calmodulin, PLCgamma, IP(3) receptors, and with scaffolding proteins like InaD, EBP50/NEHRF, caveolin, Janctate and Homers.
自上世纪最后几年被发现以来，哺乳动物瞬时受体电位（经典型）（TRPC）通道一直备受关注，它们是由激素、生长因子和神经递质通过激活PLC发挥作用而激活的Ca(2+)进入途径的主要候选者。尽管TRPC通道已被明确证明至少在一定程度上介导了几乎所有细胞类型中受体激活的Ca(2+)内流，但在使用重组通道的表达系统中记录的它们的几个核心特征与天然受体依赖性Ca(2+)流入通道的特征不同。本综述试图强调TRPC通道与其他蛋白质的相互作用，这可能解释了在天然和重组通道中观察到的TRPC通道激活和调节机制的变异性。这些相互作用包括TRPC通道亚型的同源和异位相互作用、TRPC通道与钙调蛋白、PLCγ、IP(3)受体以及与InaD、EBP50/NEHRF、小窝蛋白、Janctate和Homers等支架蛋白的相互作用。
