Chemistry and Biochemistry

Ken A. Christensen

Ken Christensen

Office: C205 BNSN
Office Phone: 801-422-0249
Lab Room: E241BNSN, E261 BNSN
Lab Phone: 801-422-8575
Office Hours


BS Chemistry, Brigham Young University (1992)

PhD Chemistry, University of Michigan (1997)

Postdoctoral Fellow studying Host-Pathogen Interactions with Stanley Joel Swanson, University of Michigan Medical School, Ann Arbor (1998-2002)

Postdoctoral Fellow studying Protein-Protein Interactions with John Collier, Harvard Medical School, Boston, MA (2002-2004)

Curriculum Vitae


The Christensen Lab works in the fields of biochemistry and bioanalytical chemistry. The Christen lab develops methods that apply optical spectroscopy, time-lapse microscopy, and other current analytical and biophysical techniques to questions in biochemistry, biophysics, cell and microbiology. 

A current area of research in the Christensen Lab grew out of our discovery several years ago that the anthrax toxin receptors capillary morphogenesis gene protein 2 (ANTRX2/CMG2) and tumor endothelial marker 8 (ANTRX1/TEM8) were involved in angiogenesis in pathological conditions in the eye and in tumor models. The Christensen Lab Group developed and used fluorescence resonance energy transfer (FRET)-based high throughput screening assays aimed at identifying molecules that block protein-protein interactions with anthrax toxin receptors. Small molecules that were identified in this screen continue to be developed as potential therapeutics for corneal neovascularization and other pathologies of angiogenesis. The Christensen Group has recently begun using phage display technology to identify short peptide sequences with similar antiangiogenic effects. In parallel with these discovery efforts, Christensen researchers are working to identify the native role of CMG2 and TEM8 and how these receptors interact with extracellular matrix proteins. The Christensen Lab believes that this may be important to understand the receptor’s roles in important signaling pathways of angiogenesis.

A second project focuses on measuring and monitoring glucose metabolism in eukaryotic parasites.  For example, in Trypanosoma brucei (the causative agent of Human African Trypanosomiasis), the sole source for generating ATP during the infectious lifecycle stage of the African trypanosome occurs exclusively in a unique peroxisome-like compartment called the glycosome. The Christensen Lab is developing and using both recombinant protein-based FRET sensors and peptide-targeted small molecule sensors to quantitatively measure intraglycosomal pH, glucose, and ATP levels in live parasites. Christensen researchers are interested in the mechanisms the organism uses for regulation of pH, glucose, ATP production, and other important metabolites. Since glycolysis is key to parasite survival, inhibiting glycolysis in the glycosome could be an excellent targeted therapeutic approach for treatment of African Trypanosomiasis.  Other parasites of particular interest to the Christensen Lab are Leishmania donovoni and Trypanosoma cruzi.