Theodore F. Taraschi, PhD
Jefferson Alumni Hall, Suite M41-F
Philadelphia, PA 19107
Most Recent Peer-reviewed Publications
- Defining the morphology and mechanism of the hemoglobin transport pathway in Plasmodium falciparum-infected erythrocytes
- Malaria drug resistance is associated with defective DNA mismatch repair
- The longin domain regulates the steady-state dynamics of sec22 in plasmodium falciparum
- A new model for hemoglobin ingestion and transport by the human malaria parasite Plasmodium falciparum
- Expression and biochemical characterization of the Plasmodium falciparum DNA repair enzyme, flap endonuclease-1 (PfFEN-1)
PhD, Rutgers University, Chemistry - 1980
Associate Provost for Research Support Services
Pathology, Anatomy & Cell Biology
Research and Clinical Interests
The invasion of erythrocytes by Plasmodium falciparum parasites produces aninfection that causes major changes in the structure, composition, antigenicity and function of the host cell membrane. During infection, the parasite actively imports obligate nutrients from the serum and exports lipids, proteins and membranes to the erythrocyte cytoplasm and the erythrocyte membrane. The regulation of these pathways must be underparasite control since mature erythrocytes have limited lipid synthetic or metabolic capabilities and do not have the machinery to synthesize or process proteins. Elucidation of trafficking pathways is complex in Plasmodia-infected erythrocytes compared to other eukaryotic cells, since the parasite is separated from the serum by its plasma membrane, the parasitophorous vacuolar membrane PVM and the erythrocyte membrane. There remains a long-felt need to identify the cellular components of these trafficking pathways to gain a better understanding of transport mechanisms in malaria-infected erythrocytes.
The laboratory is engaged in three areas of inquiry:
- Elucidation of parasite protein trafficking pathways from intracellular parasites to the erythrocyte cytosol and host cell membrane.
- Determination of the mechanism of hemoglobin uptake and transport by intraerythrocytic parasites
- Characterization of parasite DNA repair pathways (e.g. base excision and mismatch repair). Continued identification of the cellular components of these trafficking pathways to gain a better understanding of transport mechanisms in malaria-infected erythrocytes.