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Cell Communication & Adhesion Volume 8, 2001 - Issue 4-6
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Original Article

Protein Kinase C-Epsilon Mediates Phorbol Ester-Induced Phosphorylation of Connexin-43

B. W. Doble Institute of Cardiovascular Sciences and Departments of Human Anatomy and Cell Sciences, and Physiology, University of Manitoba, Winnipeg, Manitoba, Canada
,
P. Ping University of Louisville, KY, USA
,
R. R. Fandrich University of Louisville, KY, USA
,
P. A. Cattini University of Louisville, KY, USA
&
E. Kardami Institute of Cardiovascular Sciences and Departments of Human Anatomy and Cell Sciences, and Physiology, University of Manitoba, Winnipeg, Manitoba, CanadaCorrespondence[email protected]
Pages 253-256 | Received 01 Sep 2001, Accepted 15 Sep 2001, Published online: 11 Jul 2009

References

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  • Dempsey E. C., et al. Protein kinase C isozymes and the regulation of diverse cell responses. Am. J. Physiol. Lung Cell Mol. Physiol. 2000; 279: L429–38
  • Doble B. W., et al. Fibroblast growth factor-2 decreases metabolic coupling and stimulates phosphorylation as well as masking of connexin43 epitopes in cardiac myocytes. Circ. Res. 1996; 79: 647–658
  • Doble B. W., et al. The epsilon subtype of protein kinase C is required for cardiomyocyte connexin-43 phosphorylation. Circ. Res. 2000; 86: 293–301
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  • Ping P., et al. Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits: a signaling mechanism for both nitric oxide- induced and ischemia-induced preconditioning. Circ. Res. 1999; 84: 587–604
  • Ping P. J., et al. PKC-dependent activation of p44/p42 MAPKs during myocardial ischemia-reperfusion in conscious rabbits. Am. J. Physiol. 1999; 276: H1468–481
  • Ping P., et al. Functional proteomic analysis of protein kinase C epsilon signaling complexes in the normal heart and during cardioprotection. Circ. Res. 2001; 88: 59–62
  • Saez J. C., et al. Regulation of gap junctions by protein phosphorylation. Braz. J. Med. Biol. Res. 1998; 31: 593–600

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