Naik Research

Contact

Name: Ulhas P. Naik, PhD
Position:
  • Director, Cardeza Center for Vascular Biology
  • Professor of Medicine
Organization: Department of Medicine, Division of Hematology
Contact Number(s):

The Naik laboratory is focused on developing therapeutic strategies to interrupt the progress of cardiovascular diseases and cancer, which are the leading causes of death in the western world. In this regard, the team has identified several novel gene products that play key regulatory roles in the progression of these diseases, with an emphasis on how these genes affect platelet functions (since platelet activity often potentiates these diseases). Using cell and molecular biological approaches, the team has characterized the potential role of calcium- and integrin-binding (CIB) protein family and junctional adhesion molecule (JAM) family members in physiological and pathological settings. Cutting edge technologies, such as the yeast two-hybrid system, siRNA, transgenic mouse models, CRISPR/Cas9, and in vivo disease models are routinely employed in the laboratory. Dr. Naik is also the Director of the Cardeza Center for Vascular Biology, and a member of the following Graduate Programs: Genetics, Genomics and Cancer Biology; Cell Biology and Regenerative Medicine; and Biochemistry and Molecular Pharmacology, and Molecular Physiology & Translational Medicine.

Research Projects

Positive & negative regulatory mechanisms of platelet activation during thrombosis

Our team has identified numerous novel regulators of platelet activity genetic ablation of which has shown protection from thrombosis (e.g. Cib1 [Naik MU, et al., 2009] and Ask1 [Naik MU, et al., 2017]) or amplification of platelet function (e.g. JAM-A [Naik MU, et al., 2012]). For example, the adjacent image from Naik MU, et al., 2017 shows how in a model of pulmonary thromboembolism, whereby clots are induced to form in the tail vein and subsequently lodge in the lungs leading to breathing cessation, Ask1 knockout mice have a much higher survival rate than their wildtype counterparts; hence deletion of Ask1 protects from thrombosis. Currently, several other genes products are being investigated through exciting in vitro, ex vivo, and in vivo methods, including carotid artery injury, cremaster injury, stroke, and Deep Vein Thrombosis models.

Current Projects

  • 1R01 HL173436
  • AHA Postdoctoral Fellowship 26POST1568796 to Dr. Manjuprasanna Voddarahalli Nagaraju