The essential role of gap junctional intercellular communication in the normal functioning of cells and its relationship to disease is only beginning to be understood. Gap junction channels assemble when connexins oligomerize into a connexon or hemichannel and dock with a connexon from a neighboring cell. These channels cluster at defined cell-cell contacts to form gap junctions. It is now apparent that most human cells express more than one of the 21 members of the connexin family. Therefore, in addition to homomeric, homotypic and homocellular gap junctions, a diverse arrangement of heteromeric, heterotypic and heterocellular gap junctions exist between contacting cells. The complexity of channel constituents and arrangements within tissues is thought to be critical in selective passage of small biological molecules, like secondary messengers, from one cell to another. Interestingly, the generation of connexin null mice has revealed a number of defects ranging from embryonic lethal to relatively normal animals. These findings highlight the importance of connexins in nearly every major organ in the body. In the last couple of decades, mutations in the genes encoding several members of the connexin (Cx) family of gap junction proteins have been linked to a number of human diseases including a wide array of skin diseases and developmental disorders, all of which are currently under investigation in the Laird laboratory.
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