This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The overall goal of these studies is to understand how the regulation of intercellular gap junctional communication (GJC) contributes to the regulation of cell growth. We will specifically examine the regulation of the connexin 43 (Cx43) gap junction protein by mitogen-induced phosphorylation and novel Cx43-interacting proteins. Cx43 has been termed a 'tumor suppressor' due to its association with decreased rates of cell growth, a property thought to be mediated by the intercellular exchange of growth regulatory signals through gap junctions. Stimulation by growth factors or expression of viral oncogenes in normal cells is associated with increased Cx43 phosphorylation and altered GJC. The v-Src oncoprotein directly phosphorylates Cx43 on tyrosine, whereas activation of the epidermal growth factor receptor initiates activation of the mitogen-activated protein kinase (MAPK) signaling cascade and MAPK-mediated serine phosphorylation on Cx43.
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