Molecular Cell Biology Group
Our research group studies the molecular mechanisms underlying tumor suppression, with focus on the role of intercellular communication. One important mechanism for intercellular communication involves the direct transfer of signaling molecules between neighbouring cells via intercellular channels. These channels are assembled in specialized plasma membrane domains called gap junctions. Gap junctions play important roles in a variety of cellular processes, including cell growth control and differentiation. A large body of experimental evidence indicates that loss of gap junctional intercellular communication is an important step in cancer development.
Gap junction channels consist of a family of trans-membrane proteins called connexins. Several members of the connexin protein family have been shown to function as tumor suppressor proteins, and are potential biomarkers and targets for chemoprevention. We aim to elucidate the mechanisms involved in down-regulation of connexins during cancer development, and to understand the molecular basis underlying their role as tumor suppressors.
The group is member of "CoE - Centre for Cancer Biomedicine".
| RESEARCH THEMES |
Role of connexins in colorectal cancer
Post-translational modifications of Connexin43 in carcinogenesis
Role of connexins in chemical carcinogenesis
Group contact information
Oslo University Hospital HE - Norwegian Radium Hospital
Mail address: P. O. Box 4953 Nydalen, NO-0424 Oslo, Norway
Street address: Norwegian Radium Hospital, Montebello
Phone: +47 22 78 17 18, Switchboard: +47 22 93 40 00
Email: edgar.rivedal@rr-research.no
May 8, 2012
Latest publications
Molecular Cell Biology Group
The Gap Junction Channel Protein Connexin 43 Is Covalently Modified and Regulated by SUMOylation
J Biol Chem, 287 (19), 15851-61
PubMed 22411987
Endocytosis and post-endocytic sorting of connexins
Biochim Biophys Acta (in press)
PubMed 21996040
Quantitative validation of GJC1 promoter hypermethylation in benign and malignant colorectal tumors
Endocr Relat Cancer, 18 (6), C31-4
PubMed 21868474
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