Fig. 8. Illustration of the molecular dynamics of the interactions of Cx43, ZO-1 and Src during endocytic internalization of gap junction plaques in response to treatment with HCH. If a sufficient amount of activated Src is present in pathological tissues or in cells that were treated with carcinogen, dissociation of the Cx43–ZO-1 complex occurs after the kinase Src associates with Cx43, rapidly resulting in both internalization of the gap junction plaque and formation of the annular gap junction. The reduced level of ZO-1 on one side of the Cx43 gap junction plaque at the beginning of internalization could be indicative of the cell that endocytes the gap junction plaque.