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M. Cohen-Armon

M. Cohen-Armon

Tel-Aviv University


Education in theTechnion, Israel, B.Sc. Chemistry (cum laude) and D.Sc., Biophysics & Electrophysiology. Academic position at the Tel-Aviv University Life Science, Neurobiochemistry, and 1992-present: Faculty of Medicine, Dept. of Physiology and Pharmacology. On 2001, she was a visiting researcher in Columbia University, New York, lab of Learning and Memory, in collaboration with Late Prof. James Schwartz. Prof Cohen-Armon is an academic editor in PLOS ONE and Am. J. of Alzheimer's Disease & Other Dementias, She is the recipient of numerous professional awards including HFSP. She authors several high impact papers. Her discovery on the voltage dependence of GPCR affinity for their agonists (reported in PNAS and J Biol Chem) developed into a new research field. On 2004 Dr Cohen-Armon and Prof Schwartz first reported on a mechanism in the chromatin that is required for long-term memory acquisition during learning. Their finding was reported in Science, and was accompanied by Press release in USA and Israel. Their discovery lead to the disclosure of epigenetic mechanisms underlying addiction. Through 2000-2007 Dr Cohen-Armon identified the role of the chromatin-bound protein PARP1 in signal transduction mechanisms evoking gene expression in response to excitatory signals (reported in J Cell Biol, J Neurosci, Mol Cell, TIPS). The implication of this molecular mechanism in synaptic plasticity and long-term memory is the main topic of her current research. On 2009 Dr Cohen-Armon discovered that human solid cancer cells are exclusively eradicated by a small molecule, the phenanthridine PJ34, which protects human normal cells from apoptotic cell death. She identified the exclusive death mechanism activated by this molecule in human cancer cells during mitosis. Her finding was accompanied by a word wide press release, and was patented. At present, her applied research on PJ34 is supported by Novartis.

Research Interest

Topics of interest: Signal transduction, Epigenetic mechanisms, PARP1 and polyADP-ribosylation; Molecular mechanisms mediating long-term memory formation during learning; Memory erasure; A selective eradication of human cancer cells.