My primary research interest lies in unraveling the molecular mechanism of metastasis-associated PRL-3 phosphatase using biochemical approaches, supplemented with relevant tumor mouse models. The goal of this on-going study is to identify potential intervention points in PRL-3-driven cancer progression, as well as new therapeutic approaches in targeting this oncogene.

My projects in the Cohen lab focus on roles for microRNAs in the Drosophila CNS. Broadly speaking, my interests are in understanding brain development, and how development influences CNS functions. I chose the fly model as its available genetic tools makes it possible to thoroughly investigate a neurobiological question in one system, from a molecular developmental phenotype to subsequent physiological and behavioral characterization. The fly is becoming a surprisingly good model for several types of human nervous system disorders, and a final interest is to use fly models to better understand human CNS diseases. My PhD dissertation work at Harvard Medical School examined roles for potassium channels in left-right patterning and eye development, carried out in the lab of Dr. Michael Levin.

My research interest focuses on tight junctions and related proteins. Currently, I am working on the Y-box transcription factor, ZONAB (ZO-1-associated nucleic acid-binding protein), that binds to the SH3 domain of ZO-1, a submembrane protein of tight junctions. We have found in our ZONAB knockout male mice a decrease in fertility and are currently trying to elucidate the role of ZONAB with regards to spermatogenesis.

Our lab is interested in the regulation of trafficking events at the Golgi, and their consequences on cellular physiology and function. An RNAi screen of Golgi morphology previously performed in the lab found that a sizeable portion of the kinome regulates Golgi organization. My research focuses on one of the interesting hits from the screen, an Eph receptor, which belongs to a family of proteins important in development as well as in cancer. Knockdown of this Eph receptor changes Golgi morphology and glycosylation, and the goal of my work is to elucidate the mechanism by which this occurs, as well as the functional consequences of this regulation.

Prostate cancer is the second leading cause of cancer deaths in America men, following lung cancer. Though rare in young males below 40 years old, it is very prevalent in older males. My research focuses on identifying and studying genes that are up- or down-regulated in prostate cancer. We hope to be able to identify key players that are involved in the tumorigenesis process in contribution to the development of detection and treatment of the disease.

My current research interest lies in the phenomenon of EMT (Epithelial-Mesenchymal Transition) and its possible link to cisplatin resistance in ovarian cancer cells. We hope to elucidate potential EMT players which have a significant role in cisplatin resistance. The focus of my Ph.D research was the role of LPA1 (lysophosphatidic acid receptor 1) in the effects of prenatal hypoxia on fetal brain development, and was conducted in the lab of Dr. Jerold Chun at the Scripps Research Institute, California.

Hippo signaling pathway has been implicated in the regulation of organ size by promoting apoptosis (programmed cell death). When the delicate control of organ size is disturbed, cell proliferation goes uncheck and tumors form. While there are several proteins involved in the pathway, they can be grouped into three components: the upstream regulatory factors, the kinase core and the downstream transcriptional machinery.
The aim of my research is to use structural biology techniques to shed light on the regulation and functions of the various proteins in the Hippo pathway.

I am currently studying the role of the protein arginine methyltransferases PRMT5 and PRMT7 in normal hematopoiesis and in Myc-induced lymphomas. My Phd research focused on the network of Myc-driven oncogenic processes in prostate carcinogenesis and was carried out in the lab of Angelo M De Marzo, MD, PhD, at the Johns Hopkins University School of Medicine, USA.

My research interest is the evolution of transcriptional regulatory elements in the genomes of distantly related vertebrates. Using whole-genome comparisons of species like mammals and fish, transcriptional regulatory elements can be identified as noncoding elements that remain highly conserved over long evolutionary periods. These noncoding elements are analyzed for patterns of divergence in different genomes and their functions are characterized in transgenic assays.

My research interest is on characterizing a novel quorum sensing system in the opportunistic human pathogen Pseudomonas aeruginosa. I have previously discovered that this new system utilizes a unique class of molecules for communication – the non-ribosomal peptides – and that it plays a significant role in the regulation of virulence determinants of P. aeruginosa, especially so in conditions that mimic closely to chronic human infection. Efforts are currently made to delve deeper into the intricacies of this new system and its mechanisms.

I work with Dr Jacqueline Veltmaat to study the cellular and molecular mechanisms that regulate mammary gland development in the mouse embryo. In particular, I’m studying the roles of the Hedgehog transcription factor, Gli3 in each of the 5 pairs of mammary rudiments (MRs). Intriguingly, the loss of Gli3 results in a variety of phenotypes in the mammary rudiments: the lack of induction of MR3 and MR5, hypoplasia of MR2 and MR4, additionally aberrant morphology of MR2, and a normal MR1 (see also Lee et al, PLoS One, 2011). This, and evidence from other mouse models, show that the functionally-identical mammary rudiments are actually molecularly distinct, underscoring the importance of mammary rudiment-specific comparisons in research. On-going efforts are focused on understanding the downstream interactors of Gli3. We hope that this line of research will also lead to a greater understanding of the pathogenesis of breast anomalies and cancer.

My research interest focuses on using the zebrafish as a model organism to elucidate mechanisms that orchestrate human development and diseases. In particular we have established an in vivo zebrafish angiogenesis and metastasis model which will help us to better understand the processes and signalling pathways that govern cancer development. Cancer metastasis is a process defined by the spread of disseminated tumour cells from the primary tumour site to other distal organs via the blood or lymphatic systems. This leads to the growth of secondary micrometastasis in organs such as the liver, bone, lungs and colon.
One of the challenges that we faced when we study cancer development is that it is extremely difficult to monitor and track how cancer cells invade into the blood vessels in humans. In fact, this is hardly achievable in any other model organisms.

My current research interest is in the area of metabolic diseases, particularly insulin resistance. It is known that protein kinases are involved in insulin resistance. The goal is to use structural biology and computational methods to identify potential kinase inhibitors, for structure-based drug design. My PhD research focused on using X-ray crystallography and biochemical methods to elucidate the structure and molecular mechanism of several proteins.

Cyclin-dependent kinases (Cdks) are serine/threonine kinases whose catalytic activities rely on their association with specific cyclin subunits. Making use of mice bearing one or more targeted disruption in genes encoding for Cdks, our lab aims to extend the existing knowledge on mammalian cell cycle control. Specifically, my projects revolve around understanding how Cdks regulate the balance between proliferation and differentiation of neural precursors during embryonic brain development, a function which is vital for the proper development of a multi-layered cortex.

Phox(PX) domain-containing sorting nexins(SNXs) are emerging as important regulators of endocytic trafficking. Of the 33 mammalian SNXs that have been discovered, SNX27 is unique as it contains a PDZ domain. In order to study the physiological function of SNX27, we have produced mice homozygous for a null mutation of SNX27 by gene targeting. SNX27-/- mice displayed severe growth retardation and all died within one month of age. I am particularly interested in the neurobiological role of SNX27 in glutamate receptor trafficking.

Telomeric proteins are known to be important for telomere maintenance and chromosome end protection. However, recent evidence suggests that these proteins may also have extra-telomeric roles such as the regulation of DNA damage repair and gene transcription at non-telomeric regions. We hypothesize that these proteins may also directly regulate inflammation and are investigating the possible involvement of telomeric proteins in NFκB signaling.

The major bottleneck in the field of ovarian cancer treatment lies in the development of cisplatin chemo-resistance in patients, and ways to circumvent this problem still remain a major goal of anti-tumor therapy. The aim of my research is to employ a cisplatin dependent synthetic lethal screen to identify genes targets in tumor cells conferring chemoresistance, which might generate potential gene targets for future therapy regarding chemoresistance. Furthermore, identification of these chemosensitive loci would aid in understanding the possible role of EMT in the conferrance of chemoresistance.

My current research interest lies in the study of the Runx family genes in hematopoiesis and leukemogenesis.  The Runx family genes encode transcription factors which are involved in development and human diseases.  The RUNX1 gene is one of the most frequently mutated genes in human hematological malignancies and is a critical factor for the generation and maintenance of hematopoietic stem cells (HSCs).  Runx1 regulates the expression of stemness- and niche-related factors, such as Bmi1, CXC chemokine receptor 4 (Cxcr4) and integrin α2 (Itga2).  Deregulation of these genes is considered to be a mechanistic basis for leukemogenesis.  Another Runx family gene, Runx3, is known to be expressed in hematopoietic cells.  However, the role of Runx3 in hematopoiesis remains poorly understood.  Based on literature research and preliminary data, I hypothesize that Runx3 plays a role in hematopoiesis and leukemogenesis

Cells frequently incur cellular damage during its life time. Eukaryotic cells have evolved surveillance mechanisms, known as the checkpoint controls, to detect such damages. One such mechanism, the DNA damage checkpoint, inhibits cell cycle progression in response to DNA damage and causes cells to arrest in G2/M. This allows cells to repair the damage. However, in the instances when repair response cannot be mounted, cells escape the checkpoint arrest and resume cell cycle progression with damaged DNA. This phenomenon is known as ‘adaptation’. Currently, I am investigating the mechanism of yeast cells adaptation to DNA damage.

Cilia are microtubule-based protrusions present on almost all vertebrate cells. Multiciliate cells (MCs) line the mammalian respiratory tract, the ependyma and the oviduct, and they contribute critically to the proper functioning of these epithelia. We in the Roy lab investigate the problem of how multiple cilia arise on the cell surface using the model organism zebrafish, in which MCs are present in the pronephric duct (the zebrafish kidney). We take two approaches, the first of which is an unbiased search for genes responsible for MC formation. We aim to perform genome-wide transcript analysis comparing MCs and mono-ciliated cells. The other is a candidate-based approach, as we test whether a recently elucidated gene required for MC formation in Xenopus, multicilin, is involved in MC formation in the zebrafish.