BSB Seminar: Molecular mechanism of glucose/lactate transport in human and malarial parasites, and beyond


Glucose and lactate are critical metabolites for most living organisms. In certain circumstances, such as during the intra-erythrocytic stage of malaria parasites and in the glycolytic cancer cells, glycolysis provides the main energy by breaking down the glucose into lactate. Since glycolysis is a fast but less efficient way to generate ATP, high-speed glucose uptake and lactate extrusion are required to maintain cellular homeostasis. Therefore, glucose and lactate transporters have become targets for anti-parasitic and anti-cancer drugs. Over the past few years, we have used a combination of biophysical and biochemical approaches to understand the mechanism of human or malarial glucose and lactate transporters. We have successfully elucidated the crystal structures of human glucose transporters (GLUTs) and Plasmodium falciparum hexose transporter (PfHT), as well as the Cryo-EM structures of human monocarboxylate transporter (MCT1) and Plasmodium falciparum lactate transporter (PfFNT). Using the molecular mechanisms of these transporters, we rationally designed novel leads to PfHT, which paves the way to further antimalarial development.


Xin Jiang obtained his Ph.D. degree from the School of Life Sciences at Tsinghua University in 2017. Following this, he underwent post-doctoral training at the Molecular Department of Princeton University before joining the BABS at UNSW as a senior research fellow in 2019. His research interests are primarily focused on the mechanistic investigation of malarial drug targets and rational drug design.