Dr. Hannink received his PhD from the University of California, San Diego in 1987 with Dr. Daniel J. Donoghue and carried out postdoctoral work at the University of Wisconsin with Dr. Howard Temin.  Dr. Hannink joined the Biochemistry Department at the University of Missouri in 1990, where he is at the rank of full professor.

Dr. Hannink's research interests are in the mechanisms of intracellular signal transduction, particularly in relationship to cancer and cancer prevention.  His current research interests center around the Keap1/Nrf2 pathway and the role of Keap1 as a sensor for electrophilic molecules and overt oxidative stress.  His lab has demonstrated that Keap1 is part of a ubiquitin ligase complex that targets Nrf2 for degradation.  Specific cysteine residues in Keap1 are modified by electrophilic compounds, resulting in reduced ubiquitination of Nrf2. Increased steady-state levels of Nrf2 result in increased expression of genes that neutralize reactive molecules, eliminate damaged proteins and restore cellular redox homeostasis. The Keap1/Nrf2 complex has a major role in cell survival in response to chemical and oxidative stress and is a good target for the development of therapeutic strategies to minimize oxidative stress and promote cell survival.