Phosphorylation of connexin43 induced by Src: Regulation of gap junctional communication between transformed cells

Madhuri Pahujaa, Michael Anikin, Gary S. Goldberg

Research output: Contribution to journalReview articlepeer-review

74 Scopus citations

Abstract

Cx43 is a widely expressed gap junction protein that mediates communication between many cell types. In general, tumor cells display less intercellular communication than their nontransformed precursors. The Src tyrosine kinase has been implicated in progression of a wide variety of cancers. Src can phosphorylate Cx43, and this event is associated with the suppression of gap junction communication. However, Src activates multiple signaling pathways that can also affect intercellular communication. For example, serine kinases including PKC and MAPK are downstream effectors of Src that can also phosphorylate Cx43 and disrupt gap junctional communication. In addition, Src can affect the expression of other proteins that may affect intercellular communication. Indeed, disruption of gap junctions by Src appears to be complex. It has become clear that Src can affect Cx43 activity by multiple mechanisms. Here, we review how Src may orchestrate events that regulate intercellular communication mediated by Cx43.

Original languageEnglish (US)
Pages (from-to)4083-4090
Number of pages8
JournalExperimental Cell Research
Volume313
Issue number20
DOIs
StatePublished - Dec 10 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology

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