Focus: Cell Death
Timothy Larocca, PH.D.
- Ph.D. in Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY
- Postdoctoral Fellowship on host cell responses and programmed cell death, Columbia University, New York, NY
COURSES TAUGHT AT ACPHS
- Microbial Physiology (undergraduate level)
- Advanced Cell Biology (graduate level)
- Advanced Molecular Biology (graduate level)
- Cell Death and Disease (graduate level)
- Dr. LaRocca’s research focuses on different forms of programmed cell death in eukaryotic cells. Programmed cell death is the controlled death of eukaryotic cells in response to specific, external stimuli or internal cellular damage. This type of cell death is not random or accidental but rather depends on defined cell signaling, occurring in an orchestrated manner. Several different programmed cell death pathways exist but apoptosis and the more recently discovered necroptosis are the major pathways with each serving as backups to one another. Dr. LaRocca focuses on the balance between apoptosis and necroptosis and is interested in identifying different stimuli and conditions that favor one form of programmed cell death over the other with the hope that this will reveal important molecular switches that control this balance. There are currently three broad projects in Dr. LaRocca’s lab that focus on programmed cell death. One project explores the effect of hyperglycemia (high glucose concentrations as in diabetes) on apoptosis and necroptosis and how this condition may shift the balance of programmed cell death. Another project aims to define programmed cell death pathways activated in response to a broad group of bacterial virulence factors called pore-forming toxins. This project also aims to explore differences in programmed cell death in response to different pore-forming toxins. The third project is a continuation of Dr. LaRocca’s previous discovery of necroptosis in human erythrocytes (red blood cells, RBCs). As RBCs are quite different from the rest of the cells in humans (they lack nuclei and mitochondria) it is of interest to explore the mechanism of this pathway in RBCs and its outcomes compared to necroptosis of nucleated cells.
- McCaig WD, Deragon MA, Haluska RJ, Hodges AL, Patel PS, and LaRocca TJ (2019). Journal of Visualized Experiments. In press.
- McCaig WD, Patel PS, Sosunov SA, Shakerley NL, Smiraglia TA, Craft MM, Walker KM, Ten VS, and LaRocca TJ. Hyperglycemia potentiates a shift from apoptosis to RIP1-dependent necroptosis. Cell Death Discovery 2018 May 10;4:55. doi: 10.1038/s41420-018-0058-1.
- Rampersaud R, Lewis EL, LaRocca TJ, and Ratner AJ (2018). Environmental pH modulates inerolysin activity via post-binding blockade. Scientific Reports 8(1):1542.
- LaRocca TJ, Stivison EA, Mal-Sarkar T, Hooven TA, Hod EA, Spitalnik SL, and Ratner AJ. (2015). CD59 signaling and membrane pores drive Syk-dependent erythrocyte necroptosis. Cell Death and Disease. 6:e1773.
- LaRocca TJ, Stivison EA, Hod EA, Spitalnik SL, Cowan PJ, Randis TM, and Ratner AJ. (2014). Human-specific bacterial pore-forming toxins induce programmed necrosis in erythrocytes. MBio. 5(5):e01251-14.
- LaRocca TJ, Sosunov SA, Shakerley NL, Ten VS, and Ratner AJ (2016). Hyperglycemic conditions prime cells for RIP1-dependent necroptosis. Journal of Biological Chemistry. 291(26):13753-61.
- Graduate standards Committee
- Molecular Biosciences Admissions Committee
- Institutional Biosafety Committee
- Academic Standards Comittee (chair)
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CONFERENCES AND PRESENTATIONS
McCaig WD, Patel PS, Sosunov SA, Shakerley NL, Smiraglia TA, Craft MM, Walker KM, Ten VS, and LaRocca TJ. Hyperglycemia potentiates a shift from apoptosis to RIP1-dependent necroptosis. Keystone Symposia Conference: Cell Death, Inflammation, and Adaptation to Tissue Stress, Breckenridge CO, January 21-25, 2018 (poster presentation).
LaRocca TJ. Hyperglycemia potentiates a shift from apoptosis to RIP1-dependent necroptosis. 21st Annual Upstate NY Immunology Conference, Cooperstown NY, October 18, 2018 (invited oral presentation).