Dr. Ingela Jansson is an Assistant Professor of Pharmacology. She received a B.A. in Pharmacy from the University of Stockholm and, after working a while as a pharmacist, reentered the University of Stockholm, earning a B.A. and M.S. in Chemistry, She then enrolled in the Ph.D. program of the University of Stockholm Department of Biochemistry, where she trained under Professor Lars Ernster. She did postdoctoral training in the Biochemistry Department at the University of Texas Southwestern Medical School in Dallas with Professor Ronald Estabrook, followed by training at Yale University School of Medicine in the Pharmacology Department with Professor John B. Schenkman. Dr. Jansson subsequently took her present position in the Department of Pharmacology at the University of Connecticut Health Center. In 1995-1998 she held a joint appointment in Laboratory Medicine and carried out collaborative studies on nickel toxicity with Dr. William Sunderman, jr. Dr. Jansson has been Emeritus since 1998, but continues to carry out research with our laboratory. She has published more than 60 peer-reviewed papers in the field of cytochrome P450 monooxygenases, has discovered and isolated new constitutive forms of cytochrome P450, demonstrated the presence of microheterogenous forms of cytochrome P450 in liver microsomes. Many of her early publications have dealt with the interactions between cytochrome b5 and cytochrome P450 forms, and the role of the interactions in enzyme turnover. Her more recent studies have dealt with heterologous expression of forms of cytochrome P450 and focused on attempts to understand the basis for orthologous forms of the hemoprotein found in vertebrates.
Dr Jansson has recently become involved in development of cytochrome P450 heterologous expression systems, and has expressed a number of mammalian forms of the enzyme in Escherichia coli. She became interested in the role of CYP1B1 in primary congenital glaucoma as the result of a collaboration initiated between our laboratory and that of Dr. Mansoor Sarfarazi. She was able to express and study this protein and identified a possible explanation for the incomplete penetrance observed in individuals with point mutations in the primary structure of this protein that did not result in truncation of the enzyme. Her data indicated that the mutated proteins often had decreased stability and/or seriously diminished turnover numbers. As pointed out in a paper published in Pharmacogenetics [11:1-9 (2001)], since the enzyme is inducible by environmental xenobiotics, in utero and postnatal exposure to such agents could lead to elevated levels of the CYP1B1 (induction), and as a result enable offspring homozygous for the mutation to escape the disease phenotype. Dr. Jansson has been seeking to learn the endogenous substrate of the orthologous CYP1B1 hemoproteins, and has examined steroids of the different classes, fatty acids and retinoids as potential substrates with roles in mammalian development. Her studies interdigitate with those of Dr. Dharamainder Choudhary, who has become a new addition to the faculty ranks. Some of her recent studies are listed in her biosketch, below, and described in the laboratory research pages.