Enhanced connexin 43 expression delays intra-mitotic duration and cell cycle traverse independently of gap junction channel function

Scott R. Johnstone, Angela K. Best, Catherine Wright, Brant Isakson, Rachel J. Errington, Patricia E.M. Martin

Research output: Contribution to journalArticle

Abstract

Connexins (Cxs) and gap junction (GJ)-mediated communication have been linked with the regulation of cell cycle traverse. However, it is not clear whether Cx expression or GJ channel function are the key mediators in this process or at what stage this regulation may occur. We therefore tested the hypothesis that enhanced Cx expression could alter the rate of cell cycle traverse independently of GJ channel function. Sodium butyrate (NaBu) or anti-arrhythmic peptide (AAP10) were used to enhance Cx expression in HeLa cells stably expressing Cx43 (HeLa-43) and primary cultures of human fibroblasts (HFF) that predominantly express Cx43.

Original languageEnglish
Pages (from-to)772-782
Number of pages11
JournalJournal of Cellular Biochemistry
Volume110
Issue number3
DOIs
Publication statusPublished - Jun 2010

Keywords

  • connexins
  • gap junctions
  • wound healing

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