Mutations in several members of the connexin (Cx) family of gap junction proteins have been linked to a number of human diseases including congenital deafness, Charcot Marie Tooth disease, various skin diseases, and oculodentodigital dysplasia. Our lab currently has four major areas of interest: Gap junctions in breast cancer Connexin trafficking and assembly Disease-causing connexin mutationsLaird Laboratory Research
Gap Junction Background
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 cells express more than one of the 20 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.
