Nicolas Nassar, PhD
- Member, Division of Experimental Hematology & Cancer Biology
- Associate Professor, UC Department of Pediatrics
About
Biography
My areas of research interest include drug development and signaling with focus on small GTPases. My research is both basic and translational.
My research efforts encompass several methodologies, including protein crystallography, biophysical and biochemical studies, cellular functional assays, and ultimately, identifying small molecule compounds that bind to and modulate GTPase signaling in in vivo models of cancer.
Rac GTPases are key regulators of cell growth. By reorganizing the actin cytoskeleton in response to extracellular cues, Rac GTPases play a key role in cancer cell metastasis. My lab's goal is to understand the regulation of Rac and its role in cancer. More specifically, my work aims to find ways to inhibit its hyperactivation in leukemia.
One of my lab’s groundbreaking discoveries is the identification of a small molecule inhibitor of Vav3, a Rac activator. Our research aims to unravel the mechanism of action of the Vav3-inhibitor. In addition, our small molecule technology has been submitted to the US Patent Office.
My research has been published in PLoS ONE, Leukemia, JCI Insight, and Oncogene: Including Oncogene Reviews. I have been a researcher for more than 20 years and began working at Cincinnati Children’s in 2010.
PhD: University Joseph Fourier, Grenoble,France, 1992.
Postdoc: Max Plank Institut, Dortmund, Germany, 1996.
Research Associate: Cornell University, Ithaca, NY, 2000.
Assistant Professor: Stony Brook University, NY, 2006.
Research Assistant Professor: Stony Brook University, Stony Brook, NY, 2010.
Research Areas
Experimental Hematology and Cancer Biology, Cancer and Blood Diseases
Publications
Merlin tumor suppressor function is regulated by PIP2-mediated dimerization. PloS one. 2023; 18:e0281876.
VPS4A Mutations in Humans Cause Syndromic Congenital Dyserythropoietic Anemia due to Cytokinesis and Trafficking Defects. The American Journal of Human Genetics. 2020; 107:1149-1156.
IODVA1, a guanidinobenzimidazole derivative, targets Rac activity and Ras-driven cancer models. PloS one. 2020; 15:e0229801.
Breast cancer-associated missense mutants of the PALB2 WD40 domain, which directly binds RAD51C, RAD51 and BRCA2, disrupt DNA repair. Oncogene: Including Oncogene Reviews. 2014; 33:4803-4812.
Direct inhibition of retinoblastoma phosphorylation by nimbolide causes cell-cycle arrest and suppresses glioblastoma growth. Clinical Cancer Research. 2014; 20:199-212.
Sts-2 is a phosphatase that negatively regulates zeta-associated protein (ZAP)-70 and T cell receptor signaling pathways. The Journal of biological chemistry. 2011; 286:15943-15954.
The 1.35 A resolution structure of the phosphatase domain of the suppressor of T-cell receptor signaling protein in complex with sulfate. Acta Crystallographica. Section F: Structural Biology Communications. 2010; 66:643-647.
Structure of the dominant negative S17N mutant of Ras. Biochemistry. 2010; 49:1970-1974.
From the Blog
Small Molecule IODVA1 Shows Early Promise Against RAS-Driven Cancers
Nicolas Nassar, PhD3/16/2020
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