{"id":18,"date":"2017-02-06T10:48:16","date_gmt":"2017-02-06T15:48:16","guid":{"rendered":"https:\/\/health.uconn.edu\/synapse\/?page_id=18"},"modified":"2026-03-06T14:35:36","modified_gmt":"2026-03-06T19:35:36","slug":"lab-members","status":"publish","type":"page","link":"https:\/\/health.uconn.edu\/synapse\/lab-members\/","title":{"rendered":"Lab Members"},"content":{"rendered":"

David C. Martinelli, Ph.D.<\/h4>\n

\"David<\/h4>\n

Associate Professor of Neuroscience<\/span><\/p>\n

Location: L4003<\/p>\n

Phone: 860-679-2271<\/p>\n

Email: davidmartinelli@uchc.edu<\/a><\/p>\n

Profile<\/a><\/p>\n<\/div><\/div><\/div><\/div>

\u00a0<\/p>\n

David Martinelli received his Bachelor of Science degree in molecular genetics from the University of Rochester graduating summa cum laude. During this time, he spent one semester studying abroad at the University of Adelaide in Australia and one summer at Pfizer Pharmaceuticals in Groton Connecticut studying embryonic stem cells.<\/p>\n

For graduate school, he attended the Johns Hopkins University and joined the laboratory of Dr. Chen-Ming Fan at the Carnegie Institution for Science, Department of Embryology. In the Fan lab, David Martinelli studied the sonic hedgehog signaling pathway, an essential pathway involved in the development of numerous tissues and organs and implicated in the progression of many cancers. He discovered that the hedgehog binding protein GAS1 enhances hedgehog signaling and transforms hedgehog protein gradients into the observed morphogenic activity gradients that specify different cell fates. This work had broad implications, as every developmental and cancerous context involving hedgehog signaling would be modified by GAS1 expression.<\/p>\n

In 2009 for his post-doctoral work, he switched fields into neuroscience, joining the laboratory of 2013 Nobel laurate Thomas Sudhof at Stanford University. There, Dr. Martinelli studied the formally orphaned G protein-coupled receptor (GPCR) BAI3 and identified C1Q-like (C1QL) proteins as the specific ligand that interacts with BAI3 and functions to promote excitatory synapse formation and maintenance. His extensive genetics studies on C1ql3<\/em> knockout mice demonstrated that they had a variety of behavioral phenotypes and may serve as a model system for multiple neuropsychiatric diseases such as ADHD and addiction predisposition. Moreover, his mechanistic studies provided the first evidence that C1QL3 regulates synapse maintenance in vivo<\/em>, by identifying a defined brain circuit controlling emotional memory that is dependent on C1QL3-positive synapses. As a whole, his work establishes C1QL proteins as novel regulators of synapses.<\/p>\n

In 2016, Dr. Martinelli joined the faculty of the Neuroscience Department at UConn Health. Here, the Martinelli lab performs basic and translational research on C1Q-like proteins and their binding partners.<\/p>\n<\/div><\/div><\/div><\/div>

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\"\"<\/a>Maksym V. Ugrak<\/strong><\/h3>\n

<\/span><\/p>\n

Graduate Assistant <\/span><\/p>\n

Location: L4008<\/p>\n<\/div><\/div><\/div>

\"\"<\/p>\n

 <\/p>\n

Keaven Caro<\/h3>\n

M.D.\/Ph.D. Student<\/p>\n

Location: L4008<\/p>\n

Email: caro@uchc.edu<\/a><\/p>\n<\/div><\/div><\/div><\/div>

Viviana Martinez<\/h3>

\"\"<\/a>
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<\/span><\/p>\n

Research Assistant <\/span><\/p>\n

Location: L4008<\/p>\n<\/div><\/div><\/div>

Daylin Gamiotea Turro<\/h3>

\"\"<\/a><\/p>\n

Research Assistant<\/p>\n

Location: L4008<\/p>\n<\/div><\/div><\/div><\/div>

Vivian Tacker<\/h3>

\"\"<\/p>\n

Research Assistant<\/p>\n

Location: L4008<\/p>\n<\/div><\/div><\/div>

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