Study by Ane Hansen Kjenseth et al. featured on the cover of Journal of Biological Chemistry
A study by PhD student Ane Hansen Kjenseth (photo) and colleagues at Department of Cancer Prevention, Institute for Cancer Research and Centre for Cancer Biomedicine, has identified a novel mechanism for regulation of intercellular communication. The article was published in the May 4 issue of Journal of Biological Chemistry, and was featured on the cover of the journal.
In the May 4 issue of Journal of Biological Chemistry, PhD student Ane Hansen Kjenseth and colleagues in Edgar Rivedal’s group at Department of Cancer Prevention, Institute for Cancer Research and Centre for Cancer Biomedicine, report that the gap junction channel protein connexin43 is covalently modified and regulated by SUMOylation. Connexin43 is the best-studied member of the connexin family, which forms intercellular channels between neighboring cells, enabling direct exchange of ions and small molecules. Intercellular communication via gap junctions plays important roles in cell growth control and tissue homeostasis, and is usually lost during cancer development. Connexins have been shown to act as tumor suppressor proteins, and are potential targets in cancer prevention and therapy. The finding that connexin43 is modified by SUMOylation is an important contribution to the understanding of the molecular mechanisms underlying the deregulation of gap junctions in cancer and other human pathologies.
The gap junction channel protein connexin43 is covalently modified and regulated by SUMOylation.
Kjenseth A, Fykerud TA, Sirnes S, Bruun J, Kolberg M, Yohannes Z, Omori Y, Rivedal E, Leithe E.
J Biol Chem. 2012 Mar 12. [Epub ahead of print] Link to PubMed