Ulhas P. Naik, PhD
Philadelphia, PA 19107
(215) 955-9170 fax
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.
Most Recent Peer-Reviewed Publications
- CIB1 protects against MPTP-induced neurotoxicity through inhibiting ASK1
- Obesity-induced endoplasmic reticulum stress causes lung endothelial dysfunction and promotes acute lung injury
- Binding of CIB1 to the aIIb tail of aIIbβ3 is required for FAK recruitment and activation in platelets
- Ask1 regulates murine platelet granule secretion, thromboxane A
2generation, and thrombus formation
- Effect of Vorapaxar Alone and in Combination with Aspirin on Bleeding Time and Platelet Aggregation in Healthy Adult Subjects
- Bacteria exploit platelets
- Junctional adhesion molecule-A suppresses platelet integrin α
IIbβ 3signaling by recruiting Csk to the integrin-c-Src complex
- Manipulating integrin signaling for anti-thrombotic benefits
- High-throughput flow cytometry screening reveals a role for junctional adhesion molecule a as a cancer stem cell maintenance factor
- Junctional Adhesion Molecule-A Regulates Vascular Endothelial Growth Factor Receptor-2 Signaling-Dependent Mouse Corneal Wound Healing
- Fucoidan is a novel platelet agonist for the C-type lectin-like receptor 2 (CLEC-2)
- Effects of JAM-A deficiency or blocking antibodies on neutrophil migration and lung injury in a murine model of ALI
- A spatial model for integrin clustering as a result of feedback between integrin activation and integrin binding
- CASK interacts with PMCA4b and JAM-A on the mouse sperm flagellum to regulate Ca2+ homeostasis and motility
- JAM-A protects from thrombosis by suppressing integrin α IIbβ 3-dependent outside-in signaling in platelets
- Calcium- and integrin-binding protein 1 regulates megakaryocyte ploidy, adhesion, and migration
- Pericyte-endothelial cell interaction: A survival mechanism for the tumor vasculature
- Contra-regulation of calcium- and integrin-binding protein 1-induced cell migration on fibronectin by PAK1 and MAP kinase signaling
- Efficient implementation of the proper outlet flow conditions in blood flow simulations through asymmetric arterial bifurcations
- Probabilistic modeling and analysis of the effects of extra-cellular matrix density on the sizes, shapes, and locations of integrin clusters in adherent cells