Src utilizes cas to block gap junctional communication mediated by connexin43

Yongquan Shen, R. Raaj Khusial, Xun Li, Hitoshi Ichikawa, Alonso P. Moreno, Gary S. Goldberg

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


The Src tyrosine kinase phosphorylates Cas (Crk-associated substrate) to confer anchorage independence and invasive growth potential to transformed cells. Gap junctional communication is often lower between aggressive tumor cells compared with normal or benign precursors. The gap junction protein connexin43 (Cx43) is a tumor suppressor that can inhibit tumor cell growth. Src can phosphorylate Cx43 to block gap junctional communication between transformed cells. However, mechanisms by which this event actually closes intercellular channels have not been clearly defined. Here, we report that Src and Cas associate with each other at intercellular junctions. In addition, Cas is required for Src to reduce dye transfer and electrical coupling between cells expressing Cx43. Thus, Src utilizes Cas to inhibit gap junctional communication mediated by Cx43. This finding introduces a novel role of the Cas focal adhesion linker protein in the gap junction complex. This observation may help explain how gap junctional communication can be suppressed between malignant and metastatic tumor cells.

Original languageEnglish (US)
Pages (from-to)18914-18921
Number of pages8
JournalJournal of Biological Chemistry
Issue number26
StatePublished - Jun 29 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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