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Tufts University School of Medicine

Athar Chishti

Professor of Developmental, Molecular & Chemical Biology
Department: Developmental Molecular and Chemical Biology
Programs: Cell, Molecular & Developmental Biology, Molecular Microbiology
Laboratory: Jaharis 701A

Athar Chishti

Professor of Developmental, Molecular & Chemical Biology
Department: Developmental Molecular and Chemical Biology
Programs: Cell, Molecular & Developmental Biology, Molecular Microbiology
Laboratory: Jaharis 701A

Phone 617-636-3457
Lab phone: 617-636-2103
Office: Jaharis 714
Campus: Boston

Links

Education

  • BS, Biochemistry, AM University
  • PhD, Biochemistry, University of Melbourne
  • Postdoctoral Training, Harvard University

Research synopsis

My primary research interest is in the assembly and regulation of the mammalian cytoskeleton. We study cytoskeletal and signaling proteins in diseases that afflict blood cells. Current topics include: (1) Mechanism of malaria parasite pathogenesis in red blood cells (RBCs) / erythrocytes. Identification of malaria parasite, Plasmodium falciparum, ligands and their cognate host receptors is essential for the development of new drugs and vaccines against malaria, a disease that kills nearly 700,000 people each year, with the majority of deaths occur in young children in sub-Saharan Africa. Recently we identified a complex of erythrocyte membrane Band 3 (anion exchanger-1 protein) and Glycophorin A as a crucial host invasion receptor for multiple parasite proteins. We are currently investigating the adhesion mechanism of infected erythrocytes, a critical event for the development of cerebral malaria. (2) We generated the first mouse models of calpain-1 and dematin deficiency, thus contributing to the mechanism of platelet tyrosine phosphatase (PTP1B) regulation and calcium mobilization. Recently, these studies led to the development of calpain-1 null Towns mouse model of sickle cell disease. Currently we are investigating calpain-1 and its substrates as potential pharmacological targets of sickle cell disease with a focus on pain, adhesion, and thrombosis. (3) We are investigating the mechanism(s) of intracellular trafficking of membrane proteins, lipids, and vesicles to specific subcellular sites via the kinesin motors. The major components of this pathway (scaffolding protein p55/MPP1, DLG human discs large tumor suppressor, and kinesin motor GAKIN/KIF13B) were identified in our laboratory from hematopoietic cells.