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Gustavo A. Arrizabalaga, PhD
Director of Trainee Recruitment, Development and Diversity in Pharmacology and Toxicology
Dr. Gustavo Arrizabalaga has been studying the cell biology of the pathogenic parasite Toxoplasma gondii for over fifteen years. He received his Ph.D. in Biology from MIT under the mentorship of Dr. Ruth Lehmann. His doctoral work focused on developmental biology and translational regulation using Drosophila as a model system. From 1999 to 2004 Dr. Arrizabalaga did a post-doctoral fellowship with Dr. John Boothroyd at Stanford University School of Medicine, where he began focusing on how Toxoplasma gondii exits its host cell. From 2004 to 2012 he was a faculty member at the University of Idaho where he established an independent research group. In 2012, he joined the Departments of Pharmacology and Toxicology and Microbiology and Immunology as an Associate Professor. He was promoted to full professor in 2017.
Panozzo-Zénere E.A., Porta E.O., Arrizabalaga G., Fargnoli L., Khan S.I., Tekwani B.L., and Labadie, G.R., 2017 A minimalistic approach to develop new anti-apicomplexa polyamines analogs, European Journal of Medicinal Chemistry
Varberg, J.M., LaFavers, K.A., 1Sullivan, W.J., 1Arrizabalaga, G., 2017 Characterization of Plasmodium Atg3-Atg8 interaction inhibitors identifies novel alternative mechanisms of action in Toxoplasma gondii, Antimicrob Agents Chemother., PMID:29158278 1Senior authors contributed equally
Garbuz, T. and Arrizabalaga, G., 2017 Lack of mitochondrial MutS homolog 1 in Toxoplasma gondii disrupts maintenance and fidelity of mitochondrial DNA and reveals metabolic plasticity, Plos One, PMID:29141004
Roiko, M.S., LaFavers, K., Arrizabalaga, G., 2017 Toxoplasma gondii-positive human sera recognize intracellular tachyzoites and bradyzoites with diverse patterns of immunoreactivity, Int J. for Parasitology.
LaFavers, K.A, Márquez-Nogueras, K.M., Coppens, I., Moreno, SNJ, Arrizabalaga, G., 2017 A novel dense granule protein, GRA41, regulates timing of egress and calcium sensitivity in Toxoplasma gondii. Cell Microb, PMID: 28430089
Colinot, D.L., Garbuz, T., Bosland, M., Rice, S., Wang, L., Sullivan, W.J., 1Jerde, T. 1Arrizabalaga, G., 2017 Toxoplasma gondii: a novel inducer of chronic prostatic inflammation and proliferative inflammatory microglandular hyperplasia in a mouse model of prostatic inflammation. Prostate, PMID: 28497488. 1 Senior authors contributed equally
Padgett, L., 1Sullivan, W.J., 1Arrizabalaga, G., 2016, Targeting of tail-anchored membrane proteins to subcellular organelles in Toxoplasma gondii. Traffic. 2017 Mar;18(3):149-158. PMID:27991712 1 Senior authors contributed equally
Charvat, R. and Arrizabalaga, G., 2016. Oxidative stress generated during monensin treatment contributes to altered Toxoplasma gondii mitochondrial function. Nature Scientific Reports, Mar 15;6. PMID: 26976749
Gaji, R., Johnson, D., Wang, M., Hudmon, A., and Arrizabalaga, G., 2015. Phosphorylation of a Myosin motor by TgCDPK3 facilitates rapid initiation of motility during Toxoplasma gondii egress. PLoS Pathog. 1(11):e1005268. PMID: 26544049
Benmerzouga, I., Checkley, L., Ferdig, M., Arrizabalaga, G., Wek, R., and Sullivan, W., 2015. Guanabenz repurposed as an anti-parasitic with activity against acute and latent toxoplasmosis, Antimicrob Agents Chemother, 59(11):6939-45. PMID: 26303803
Treeck, M., Sanders, J., Gaji, R., LaFavers, K., Child, M., Arrizabalaga, G., Elias, J., Boothroyd, J., 2014. A novel role of Calcium-dependent Kinase 3 in regulating metabolism in Toxoplasma gondii in addition to ionophore induced egress. PLoS Pathogen, 10(6):e1004197. PMID: 24945436
Gaji, R., Checkley, L., Reese, M., Ferdig, M.T., and Arrizabalaga, G., 2014. Expression of the essential kinase PfCDPK1 from Plasmodium falciparum in Toxoplasma gondii facilitates the discovery of novel antimalarial drugs. Antimicrob Agents Chemother, 58(5):2598-607. PMID: 24550330
Garrison, E., Treeck, M., Ehret, M., Garbuz, T., Oswald, B.P., Settles, M., Boothroyd, J., Arrizabalaga, G., 2012. A forward genetic screen reveals calcium-dependent kinase 3 is critical for calcium-induced egress in Toxoplasma. Plos Pathogen, 8(11). PMDI: 23209419
Lavine, M.D. and Arrizabalaga, G., 2012, Analysis of Monensin Sensitivity in Toxoplasma gondii reveals autophagy as a mechanism for drug induced death. Plos One, 7(7):e42107. PMID: 22848721
Francia, M.E., Wicher S., Pace D.A., Sullivan, J., Moreno, S.N.J., and Arrizabalaga, G., 2011. A Toxoplasma protein with homology to intracellular type Sodium Hydrogen Exchangers is required for osmotolerance and protein processing. Experimental Cell Research. 317(10):1384-96. PMID: 21501607
Lavine, M.D. and Arrizabalaga, G., 2011. The antibiotic monensin causes cell cycle disruption of Toxoplasma gondii, mediated through the DNA repair enzyme TgMSH-1. Antimicrob Agents Chemother, 55(2): 745-55. PMID: 21098240
Garrison, E. and Arrizabalaga, G., 2009. Disruption of a mitochondrial homolog of a MutS DNA Repair Enzyme confers drug resistance in the pathogenic parasite Toxoplasma gondii. Molecular Microbiology, 72(2):425-41. PMID 19291232
Arrizabalaga, G., Ruiz, F., Moreno, S. and Boothroyd J.C., 2004. Ionophore-resistant mutant of Toxoplasma gondii reveals involvement of a sodium/hydrogen exchanger in calcium regulation. Journal of Cell Biology: 165(5):653-62,. PMID: 15173192
Pharmacology & Toxicology
MS A418 635 Barnhill Drive
Indianapolis, IN 46202
Titles & Appointments
- Professor of Pharmacology & Toxicology
- Professor of Microbiology & Immunology
My research focuses on the cell signaling events that drive the propagation of the parasite. This remarkable parasite infects any warm blooded animal, can invade any nulceated cell, is found everywhere in the world, and infects a third of the world population. can cause birth defects, and opportunistic disease in HIV/AIDS, cancer and organ transplant patients. A great part of the pathogenesis associated with toxoplasmosis is due to the repeating cycles of cell invasion, replication and egress that drive its propagation through an infected individual. Our lab is interested in the signaling pathways that regulate various aspects of this lytic cycle. Given that events such as invasion and egress are essential for parasite survival and that uses some unique signaling molecules our studies aim at discovering novel targets for the development of much needed anti-parasitic drugs.
For more details about my research and ongoing projects visit my lab webpage.
Desc: Trustees Teaching Award