Ulhas P. Naik, PhD
Director, Cardeza Center for Vascular Biology
Professor of Medicine
Associate Director, Cardeza Foundation for Hematologic Research
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Ulhas P. Naik, PhD
Director, Cardeza Center for Vascular Biology
Professor of Medicine
Associate Director, Cardeza Foundation for Hematologic Research
Publications
- Small-Molecule Disruptors of the Interaction between Calcium- and Integrin-Binding Protein 1 and Integrin αIIbβ3 as Novel Antiplatelet Agents
- The Function of ASK1 in Sepsis and Stress-Induced Disorders
- Glutamate Receptor Dysregulation and Platelet Glutamate Dynamics in Alzheimer’s and Parkinson’s Diseases: Insights into Current Medications
- Illustrated Abstracts of the 5th EUPLAN International Conference
- SerpinB3 drives cancer stem cell survival in glioblastoma
Research & Clinical Interests
The focus of research in Dr. Naik’s laboratory is to understand the molecular mechanisms of cardiovascular diseases and cancer. Cell-cell interactions and cell-extracellular matrix interactions play key roles in these diseases. Dr. Naik’s research focuses on the molecular mechanisms involved in the regulation of these interactions under physiological and pathophysiological conditions, such as thrombosis, myocardial infraction, stroke, and cancer cell metastasis.
Platelets are anucleated cells circulating in the blood. They initiate the process of blood clotting under both physiological hemostasis and pathological thrombosis. Dr. Naik has cloned a novel gene, CIB1, that has been shown to play a key role in this process. Efforts are currently being directed towards understanding how CIB1 regulates the function of platelets. Efforts are now aimed to identify potential therapeutic agents that might be useful in blocking unwanted platelet clumping which may be useful in combating cardiovascular diseases such as thrombosis, myocardial infarction, and stroke.
Another research area of interest in Dr. Naik’s lab is focused on understanding the process of tumor-induced angiogenesis. Dr. Naik has cloned a novel cell adhesion molecule, JAM-A, which is involved in platelet activation, leukocyte transmigration, and in the regulation of tight junction integrity. Recent findings from Dr. Naik’s laboratory have demonstrated that JAM-A is a key player in the process of bFGF-induced angiogenesis. Presently, Dr. Naik has successfully generated JAM-A knock-out mice, which are currently being characterized phenotypically. Such studies will help delineate the molecular mechanism underlying the regulation of angiogenesis by JAM-A.
Research efforts are also being focused in understanding the molecular mechanism of breast cancer cell metastasis. Dr. Naik’s laboratory is currently elucidating the role of JAM-A and CIB1 in the process of breast cancer cell migration and invasion leading to metastasis.