Athar Chishti

Athar Chishti

(617) 636-3457
150 Harrison Ave
Research/Areas of Interest:

Our laboratory is conducting research on the assembly and regulation of the mammalian cytoskeleton with a focus on diseases that afflict red blood cells and platelets, such as malaria, babesiosis, sickle cell disease, and thrombosis. Malaria is one of the most common infectious diseases, and ~627,000 people, mostly African children, die each year due to complications of malaria (WHO Estimate for 2020). We are studying the molecular mechanisms of host-pathogen interactions in the malaria parasite infected red blood cells (iRBCs). The specific focus is on the surface protrusions called knobs in Plasmodium falciparum infected human iRBCs. Knobs are critical for the adhesion of iRBCs to host endothelial cells in the brain and placenta. Previously, we identified human erythrocyte Band 3 (anion exchanger-1 or SLC4A1) and the Glycophorin A complex as crucial co-receptors for malaria parasite surface proteins involved in the pathogen entry in host cells. Parasite proteins and their cognate host receptors are essential for the development of new therapeutics as well as an effective multi-subunit vaccine. We generated calpain-1 null mice with sickle cell disease (SCD) revealing a functional role of cysteine proteolysis in SCD and thrombosis. Additionally, our lab has generated several mutant mouse models of Dematin/Protein 4.9, P55/MPP1, Kinesins KIF13B/A, and Band 3. Some of these models are currently used for mechanistic studies in both erythroid and non-erythroid cells.


  • Bachelor of Science, A. M. University, Aligarh, IND, 1980
  • Doctor of Philosophy, University Melbourne/Australia, AUS, 1984


Our primary research interest is the assembly and regulation of the mammalian cytoskeleton, with focus on red blood cells and platelets. We study the function of cytoskeletal and signaling proteins in diseases that afflict blood cells, particularly the Plasmodium falciparum malaria, babesiosis, sickle cell disease, and thrombosis. Currently, we are investigating the molecular mechanisms of malaria parasite-infected human red blood cells adhesion to brain endothelial cells. We also study the role of the cysteine protease, calpain-1, in sickle cell disease and thrombosis. We generated the mouse models of calpain-1, p55/MPP1, dematin/protein 4.9, Band 3/Anion exchanger-1 (SLC4A1), KIF13B/GAKIN, and KIF13A deficiency, contributing to the mechanisms of lipid transport, PTP1B regulation, and calcium mobilization.