Research interests

 Our research is focused on the following projects:

1. Role of connexins in colorectal cancer
     Colorectal cancer is one of the most commonly diagnosed malignancies. In order to improve the prevention, diagnosis and therapy of colorectal cancer, it is important to identify and functionally characterize the genes involved in the development of the disease. In collaboration with Ragnhild Lothe´s research group, we are currently investigating the role of Connexin43 and other connexin isoforms in the development of colorectal cancer.

2. Post-translational modifications of Connexin43 in carcinogenesis
     Our lab is working to elucidate the mechanisms underlying post-translational regulation of Connexin43 in normal and transformed cells. We are particularly focusing on how Connexin43 is regulated by phosphorylation and ubiquitination, and the interplay between these two post-translational modifications. Regulation of connexin degradation is considered to be an important mechanism for modifying the level of gap junctions at the plasma membrane. We have previously shown that endocytosis of Connexin43 gap junctions is regulated by epidermal growth factor, and that this process involves Connexin43 ubiquitination. We are currently investigating the molecular mechanisms involved in the degradation of Connexin43, with particular emphasis on the role of ubiquitin.

3. Role of connexins in chemical carcinogenesis
     Carcinogenic substances have conventionally been divided into two categories according to their presumed mechanism of action: genotoxic or non-genotoxic. Many chemicals that cause cancer in animal studies are negative in genotoxicity assays, suggesting that these chemicals may act in a non-genotoxic manner. It is a major challenge to understand how non-genotoxic carcinogens function and to develop methods to detect such compounds in the environment. Many carcinogenic chemicals inhibit gap junction channels. The ability of chemicals to inhibit gap junctional intercellular communication is associated with their carcinogenicity, but not with their genotoxicity. We are investigating the molecular mechanisms by which chemical carcinogens inactivate gap junction channels.