2008-present Assistant Medical Professor, Sophie Davis Biomed. School, City College, CUNY, NY.
2007-2008 Adjunct Assistant Professor, Dept. of Biology, Rider University, NJ.
2000-2008 Research Associate, Dept. Molecular Biology & Biochemistry, Rutgers University, NJ
1997-1999 Post Doctoral fellow, laboratory of Dr. Monica Driscoll, Mol Bio & Biochem, Rutgers U.
Ph.D., 1996, The Weizmann Institute of Science, Rehovot, Israel
M.S., 1991, The Weizmann Institute of Science, Rehovot, Israel
B.S., 1987, Hebrew University, Jerusalem, Israel
Sophie Davis Team Taught Medical Courses
Medical Pharmacology (PA 32202, PA-program core), Medical Neurosci (MED 46800, Med-school core), Medical Pharmacology (MED 47801, Med-school core), Systemic Functions (Med. Physiol., MED 45700, Med-school core), Drug Abuse (MED 31300, a course for non-science major CCNY undergrads) Pathology for Physician Assistants (PA 32300) (guest lecturer)
CUNY Graduate Center Team Taught PhD Courses
Principles of Neuropharmacology, Cell Biology, CCNY, Molecular Biology, Neuroscience I
Other Courses Prior to Arrival to CCNY
Bio 101 for non-biology majors, Current topics in C. elegans Biology 601
I study neuronal communication that uses the key excitatory neurotransmitter Glutamate, and the process of neuronal cell death that happen when the brain is flooded with too much of it. Excessive glutamate signaling triggers the neurodegeneration seen in prevalent neurodegenerative conditions such as stroke (a condition where minority communities are at special risk) and diseases like ALS/Lau Gehrig’s disease. We understand very little about this form of neuronal cell death, and although stroke leaves a window of opportunity for intervention physicians have no effective therapies to treat it. Minority populations are especially at high risk, as African-Americans at 4 times more likely to suffer a stroke in middle age, and have an overall double the risk of death from stroke compared to Caucasians. I examine normal and pathological glutamatergic neurotransmission in the microscopic free-living nematode C. elegans, because of the strong genetic research tools available in this model system. The basic premise is that although we look very different from nematodes, we share a great similarity at the cellular and molecular levels. Therefore, if we understand basic processes of normal physiology and Glutamate-induced pathologies in nematodes, it might give us clues as to possible similar processes in people. Trained as a neuroscientist and experienced in molecular biology, electrophysiology and model-system genetics, I analyze structure-function relations in transport proteins to learn how excess Glutamate is removed from the nervous system. I use genetic tools to study what are the molecular steps that lead from Glutamate over-excitation to neurodegeneration, and I study the ability to interfere with evolutionary-conserved signaling pathways (such as cell stress or autophagy) to protect the nervous system from Glutamate-induced neurodegeneration.
Mojsilovic-Petrovic, J, Nedelsky, N, UUMano, IUU, Georgiades, SN, Zhou, W, Liu, Y, Neve, RL, Taylor JP, Driscoll M, Merry D, & Kalb, RG(2009). FOXO3a is broadly neuroprotectivein vitro and in vivo against insults implicated in motor neuron diseases.J Neurosci. 29: 8236-47.
UUMano, I.UU, and Driscoll, M., (2009) C. elegans Glutamate Transporter Deletion Induces AMPA-Receptor/Adenylyl Cyclase 9-Dependent Excitotoxicity.J. Neurochem. 108:1373-1384.
UUMano, IUU, Straud, S, and Driscoll, M (2007). C. elegans glutamate transporters influence synaptic function and behavior at sites distant from the synapse. J Biol Chem 282: 34412-9.
Hong, K. UUMano, IUU. and Driscoll, M. (2000). In-vivo structure/function analysis of C. elegans candidate mechanotransducing ion channel subunit MEC-4. J. Neurosci. 20: 2575-2588.
UUMano, IUU. and Driscoll, M. (1999). 3.0.CO;2-L/abstract">The DEG/ENaC Channels: A touchy superfamily that watches its salt. BioEssays 21 (7): 568-578.
Thieringer, H., Sahota, S., UUMano, IUU. and Driscoll, M. (1999). C. elegans degenerin channels: form and function. Curr. Top. Membr. 47: 297-314 .
UUMano, IUU. and Teichberg, V.I., (1998). A tetrameric subunit stoichiometry for a glutamate receptor/channel complex. NeuroReport 9: 327-331
UUMano, I.UU, Lamed, Y. and Teichberg, V.I., (1996). A Venus flytrap mechanism for activation and desensitization of AMPA receptors. J. Biol. Chem. 271: 15299-15302.
UUMano, .I.UU, Paperna, T., Devillers-Thiery, A., Galzi, J.-L., Changeux, J.-P., and Teichberg, V.I. (1993). A study of non-NMDA receptors in chick cerebellum. J. Neurochem. 61: S13D.
Gregor, P., Yang, X., UUMano, I.UU, Takemura, M., Teichberg, V. I. and Uhl, G. R. (1992). Organization and expression of the gene encoding chick kainate binding protein, a member of the glutamate receptor family. Mol. Brain Res. 16, 179-186.
Teichberg, V.I., Lamed Y., Maoz I., UUMano I.UU, Ortega A., Paas Y., and Paperna T. (1992). Structure and regulation of the Bergmann glia kainate receptor. in Excitatory amino acids. Fidia Res. Found. Symp. Series. Thieme Medical Publishers, 9:35-40 .
Teichberg, V.I., Eshhar, N., Maoz, I., UUMano, I.UU, Ornstein, D., Ortega, A., Gregor, P. (1990). Molecular characterization, ultrastructural localization and gene cloning of the chick cerebellar kainate receptor. Adv Exp Med Biol 268:73-78 .
Gregor, P, UUMano, IU, Maoz, I, McKeown, M & Teichberg VI(1989). Molecular structure of the chick cerebellar kainate-binding subunit of a putative glutamate receptor. Nature 342, 689-92.