Connexins were first identified in the 1970s as the molecular components of vertebrate gap junctions. Since then a large literature has accumulated on the cell and molecular biology of this multi‐gene family culminating recently in the findings that connexin mutations are implicated in a variety of human diseases. Over two decades, the terms “connexin” and “gap junction” had become almost synonymous. In the last few years a second family of gap‐junction genes, the innexins, has emerged. These have been shown to (...) form intercellular channels in genetically tractable invertebrate organisms such as Drosophila melanogaster and Caenorhabditis elegans. The completed genomic sequences for the fly and worm allow identification of the full complement of innexin genes in these two organisms and provide valuable resources for genetic analyses of gap junction function. BioEssays 23:388–396, 2001. © 2001 John Wiley & Sons, Inc. (shrink)

Intercellular communication (IC) is mediated by gap junctions (GJs) and hemichannels, which consist of proteins. This has been particularly well documented for the connexin (Cx) family. Initially, Cxs were thought to be the only proteins capable of GJ formation in vertebrates. About 10 years ago, however, a new GJ‐forming protein family related to invertebrate innexins (Inxs) was discovered in vertebrates, and named the pannexin (Panx) family. Panxs, which are structurally similar to Cxs, but evolutionarily distinct, have been shown to be (...) co‐expressed with Cxs in vertebrates. Both protein families show distinct properties and have their own particular function. Identification of the mechanisms that control Panx channel gating is a major challenge for future work. In this review, we focus on the specific properties and role of Panxs in normal and pathological conditions. (shrink)