Moreno Alonso P
Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Capitol Ave. Suite 310, Indianapolis, IN 46202, United States.
Biochim Biophys Acta. 2005 Jun 10;1711(2):164-71. doi: 10.1016/j.bbamem.2005.02.016. Epub 2005 Mar 13.
The main proteins required for functional gap junction channels are known as connexins and most of their isoforms indicate that they can become phosphorylated. Connexin phosphorylation has been reported to participate in modifying junctional communication and the mechanisms involved apparently depend on which kinase becomes involved. Although multiple reports have suggested a strong influence of phosphorylation on channel gating, not enough physiological studies have been performed to determine precisely the gating mechanisms implicated. Moreover, gap junction channels follow other various gating mechanisms, including voltage gating and chemical gating, where phosphorylation could act as a modulator. The quest for this chapter has been to discriminate those instances where phosphorylation acts directly as a gating trigger and where it acts indirectly or only as a modulator. Despite recent efforts, the mechanisms involved in all these cases are barely understood.
功能性间隙连接通道所需的主要蛋白质被称为连接蛋白,它们的大多数亚型表明其能够被磷酸化。据报道,连接蛋白磷酸化参与调节连接通讯,其涉及的机制显然取决于参与的激酶种类。尽管有多项报道表明磷酸化对通道门控有很大影响,但尚未进行足够的生理学研究来精确确定其中涉及的门控机制。此外,间隙连接通道还遵循其他各种门控机制,包括电压门控和化学门控,磷酸化在这些机制中可能起到调节剂的作用。本章的研究旨在区分磷酸化直接作为门控触发因素的情况以及它间接起作用或仅作为调节剂的情况。尽管最近进行了一些努力,但所有这些情况下涉及的机制仍几乎不为人所知。