Studies described in this dissertation have focused on understanding the crosstalk between two different classes of membrane proteins: Receptor and non-receptor tyrosine kinases and gap junctions. The first part of the study was focused on the non receptor tyrosine kinase pp60v-Src, and the various signaling pathways it utilizes to acutely inhibit Cx43 gap junctional communication. Here we have identified the involvement of at least three signaling pathways which co-coordinately regulate the acute inhibition of Cx43 coupling. The second study was directed towrards understanding the underlying principle for the transient shut down of Cx43 gap junctional communication by epidermal growth factor. Here we generated a stable clonal pool of HeLa cells expressing a growth factor insensitive mutant of Cx43 that was lacking targets for ERK phosphorylation. We looked at the changes in immediate early response of cells to EGF at the transcriptional and translational level.