{"id":69,"date":"2017-07-12T21:15:18","date_gmt":"2017-07-13T01:15:18","guid":{"rendered":"https:\/\/health.uconn.edu\/cell-biology\/?page_id=69"},"modified":"2026-03-06T07:17:40","modified_gmt":"2026-03-06T12:17:40","slug":"faculty-and-staff","status":"publish","type":"page","link":"https:\/\/health.uconn.edu\/cell-biology\/faculty-and-staff\/","title":{"rendered":"Faculty and Staff"},"content":{"rendered":"

Faculty<\/h3>\n<\/div><\/div><\/div><\/div>
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Leslie Caromile<\/strong><\/a>
\nAssistant Professor
\nCenter for Vascular Biology
\nCaromile Lab Website<\/a><\/p>\n

Research Interests:\u00a0<\/strong>My lab investigates the role of prostate-specific membrane antigen (PSMA) in prostate cancer tumor growth and metastasis, and I currently have two federally funded projects:<\/p>\n

Project 1: Recently, my lab has developed a novel multi-cell type, scaffold-free, 3D bioprinted prostatic tumor model that accurately represents the human PSMA (+) primary tumor vasculature and the primary tumor microenvironment. This model provides the laboratory with a unique system for interrogating novel PSMA small molecule inhibitors on multiple tumorigenic endpoints.<\/p>\n

Project 2:\u00a0 We are investigating if germ-line SNPs within specific components of the PSMA signaling pathway might contribute to the increased risk of prostate cancer in African American men vs. that of men of European descent. Investigation into these molecular mechanisms not only has the potential to improve the outcomes of all men with lethal prostate cancer but also can reduce prostate cancer disparities by improving detection, morbidity, and mortality of lethal prostate cancer in African American and other at-risk populations through the identification of unique, tailored treatment and prevention strategies for each patient.<\/p>\n

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Kevin Claffey<\/strong><\/a>
\nProfessor
\nCenter for Vascular Biology
\nClaffey Lab Website<\/a><\/p>\n

Research Interests:<\/strong> Breast cancer recurrence and subsequent metastasis is the cause of the majority of breast cancer related deaths. When and why breast cancer recurrence occurs also remains poorly understood. Examining the mechanisms of survival under long-term stress can provide information as to how to target these dormant cells.<\/p>\n

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Abhijit (Abhi) Deb Roy\u00a0<\/strong>
\nAssistant Professor
\nCenter for Cell Analysis and Modeling
\nDeb Roy Lab Website<\/a><\/p>\n

Research Interests: <\/strong>We are an experimental cell biology lab interested in both hypothesis-based and curiosity-driven questions, broadly within the realm of biomedical sciences. Our ongoing research projects are focused on investigating molecular signaling pathways and cytoskeletal dynamics involved in mechanobiology and cell migration. Directional cell migration plays critical roles during physiological processes such as development, angiogenesis and immune response, whereas dysregulation of cell migration is observed in pathologies such as cancer metastasis and atherosclerosis. We are interested in understanding how spatiotemporal regulation of signaling pathways modulates cytoskeletal dynamics to coordinate cell migration through diverse mechanical and biochemical environments. We employ live cell microscopy with biosensors and synthetic-biology based molecular actuators (optogenetic or chemical-inducible) to examine spatial and temporal relationships between molecular signaling pathways and cell behavior in a quantitative manner. We also collaborate with theoretical and computational biologists to develop predictive models bridging experimental observations to gain better understanding of complex biological systems.<\/p>\n

Ongoing projects:<\/strong>
\n\u2013Deciphering how post-translational modifications of microtubules, often called \u2018the tubulin code\u2019, affect their crosstalk with the actin cytoskeleton or with intermediate filaments.
\n\u2013Investigating how spatial modulation of intracellular forces affect directional cell motility.<\/p>\n

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Kimberly Dodge-Kafka<\/strong><\/a>
\nProfessor
\nPat and Jim Calhoun Cardiology Center
\nAssistant Dean for Research Planning and Coordination
\nDodge-Kafka Lab Website<\/a><\/p>\n

Research Interests:<\/strong> My research focuses on defining the intracellular communication networks that promote specificity in signal transduction. In particular, we work on A-kinase-anchoring proteins (AKAPs) that target the camp-dependent protein kinase, as well as other signaling enzymes, into discrete signaling complexes in order to regulate the phosphorylation of target proteins. In particular, we are concentrating on AKAP complexes in the heart, and how they regulate cardiac physiology.<\/p>\n

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Paul Epstein<\/strong><\/a>
\nAssociate Professor
\nEpstein Lab Website<\/a><\/p>\n

Research Interests:<\/strong> Research in the Epstein laboratory centers on second messengers and signal transduction. Particular focus has been on cyclic nucleotide metabolism and protein phosphorylation, with emphasis on analysis of cyclic nucleotide phosphodiesterases (PDEs). It has become apparent, in recent years, that PDE is a superfamily of enzymes encoded by 21 different genes, grouped into 11 gene families, based on sequence similarity, mode of regulation and preference for cAMP or cGMP as substrate. With the existence of multiple transcription initiation sites, as well as alternatively spliced forms of many of these genes, more than 100 different forms of PDE have been identified and cloned to date, and many of these PDE forms are localized to different cells and different subcellular compartments as part of complexes or signalosomes composed of scaffolding proteins, cAMP effectors, and distinct PDEs, thus achieving targeted cAMP degradation and the creation of localized intracellular cAMP gradients and allowing the control of specific cellular functions by specific PDE isoforms during cellular signaling. Hence, by inhibiting or altering the expression of specific forms of PDE, cAMP levels in specific cell types can be altered, and fundamental physiological processes in one cell type can be changed, without affecting others. Thus, a main research goal in this laboratory is to examine the tissue distribution of different forms of PDE and regulation of their expression during development and in different pathophysiological states so that specific PDE isoforms can be targeted to treat a number of different diseases. The focus of our research has been to identify and inhibit specific PDE isoforms as novel treatment methods for leukemia, breast cancer and autoimmune and inflammatory illnesses.<\/p>\n

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Guo-Hua Fong<\/strong><\/a>
\nProfessor
\nCenter for Vascular Biology
\nFong Lab Website<\/a><\/p>\n

Research Interests:<\/strong> Angiogenesis, or growth of blood vessels, is often suboptimal in many injured tissues such as ischemic tissues following heart attack or diabetic wounds. The healing and regeneration of such tissues critically depend on proper angiogenesis. On the other hand, uncontrolled neovascularization underlies many diseases such as tumor growth, diabetic retinopathy (DR), and age-related macular degeneration (AMD). In addition, capillary destruction is a significant pathological contributor to such diseases as bronchopulmonary dysplasia (BPD) and retinopathy of the prematurity (ROP). At the current state of the knowledge, the molecular mechanisms controlling angiogenesis and vascular integrity are only partially understood, which handicaps efforts to develop effective therapies. In our laboratory, we use both developmental and disease models to understand how these processes are controlled, and explore potential therapeutic approaches.<\/p>\n

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David Han<\/strong><\/a>
\nAssociate Professor
\nCenter for Vascular Biology
\nHan Lab Website<\/a><\/p>\n

Research Interests:<\/strong> The overall goal of the Han Laboratory is to utilize newly developed proteomic technologies to uncover cellular signaling networks and pathways that govern mechanisms of programmed cell death\/apoptosis. Toward the overall goal, we have made significant level of commitment to improve currently available technologies and apply proteomic technologies to uncover novel biological insights.<\/p>\n