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Barbara M. Brodsky, Ph.D. * - Piscataway - Biophysical studies on peptides which model the collagen triple-helix in various collagen types as well as in C1q, collectins, and the macrophage scavenger receptor. The effects of mutations found in genetic diseases are characterized.

Earlene B. Cunningham, Ph.D. * - Newark - Characterization and cloning a novel (human) plasma membrane-associated immunophilin (a signal transduction protein targeted by certain drugs used to prevent the rejection of organ transplants). This 12 kDa IP3-, IP4-, and phosphatidylinositol phosphate-binding protein has been named IPBP12.

Scott R. Diehl, Ph.D. * - Newark - Single Nucleotide Polymorphisms (SNPs) are analyzed to understand molecular causes of disease and individual differences in drug responses. High-throughput bioinformatics and complex statistical genetic methods are used for current research on oral cancer, periodontal disease, orofacial clefting; pharmacogenomics of pain and drug responses.

Monica, A. Driscoll, Ph.D. * - Piscataway - Our lab uses the facile C. elegans model system to investigate molecular and genetic mechanisms of necrotic cell death, aging and mechanical signalling.

Jeremy Francis, Ph.D * - Stratford - Our research seeks to determine pathogenic mechanisms underlying neurodegenerative diseases in an effort to identify avenues of therapeutic intervention. Gene and cell-based therapies are used in animal models of disease to create a foundation for possible clinical application. Email: francijs@umdnj.edu

Abram Gabriel, M.D. * - Piscataway - My laboratory focuses on the study of mechanisms and consequences of retrotransposon reverse transcription.

Grant Gallagher, Ph.D. * - Stratford - Key interests revolve around the regulation of Th2 responses in conditions such as asthma and the regulation of Th17 responses in conditions such as inflammatory bowel disease and prostate cancer. There are developing interests in systemic lupus erythematosus and first-trimester miscarriage also. The work is directed towards the development of novel diagnostic and therapeutic approaches to such conditions. Disease models are used, but primarily the research uses human cells from both healthy individuals and patients. Email: g.gallagher@humigen.org

Marc R Gartenberg, Ph.D. * - Piscataway - Large regions of eukaryotic chromosomes are heritably maintained in transcriptionally inactive states by repressive chromatin structures. Inappropriate expression of down-regulated genes can lead to cancers and other genetic diseases. We use budding yeast as a model to study how transcriptionally inactive domains are established, maintained, and propagated.

Gary, S. Goldberg, Ph.D. - Stratford - Cells must communicate with each other to coordinate the development and survival of an animal. This communication can be mediated by diffusible factors that pass between cells, or by direct contact through cell junctions. I am interested in how intercellular communication affects cell growth and differentiation, with an emphasis on how cell communication can control tumor cell growth and prevent eye diseases. Email: gary.goldberg@umdnj.edu

M. Zafri Humayun, Ph.D. * - Newark - We study mechanisms of genetic variability in Escherichia coli and in the pathogen Helicobacter pylori. We have recently defined two novel transient mutator pathways termed UVM and TSM pathways. The TSM pathway reveals unanticipated links among translation, DNA replication and recombination. Antibiotics, helicase.

Fred R. Kramer, Ph.D. * - Newark - RNA replication, RNA structure, recombinant RNA, nucleic acid probes, molecular beacons, oligonucleotide arrays

Eldo, V. Kuzhikandathil, Ph.D. * - Newark - We are interested in the molecular analysis of dopamine receptor signaling mechanisms and their role in neurological diseases.Current research projects include structure-function analysis of dopamine receptors and the developmental regulation of dopamine receptor signaling pathways.

Muriel W. Lambert, Ph.D. * - Newark - Research is ongoing on DNA repair mechanisms, in particular in cells from patients with genetic diseases with repair defects. The genes and proteins involved are being studied as is the interaction of these proteins with damaged DNA and damaged chromatin.

Robert W. Ledeen, Ph.D. * - Newark - 1. Ganglioside and sphingolipids in neuronal function: cell membrane and nuclear membrane. 2. Gangliosides as modulators of flux and signaling. 3. Myelin metabolism in multiple sclerosis and normal brain. Myelin receptors for cytokines. 4. N-Acetylaspartate and myelinogenesis.

Paola Leone, Ph.D * - Stratford - My research focus is to characterize neuropathological pathways underlying the degenerative processes associated with pediatric leukodystrophies, such as Canavan Disease, and test in vitro and in vivo novel pharmacological and stem cell applications for the development of a therapy for this disease and other leukodystrophies. Email: leonepa@umdnj.edu

Paul Manowitz, Ph.D. * - Piscataway - Identification of genes predisposing to substance abuse and other human diseases of behavior. This research includes studies of tissue culture and animal models as well as humans to elucidate the genetic, molecular biological,and biochemical bases of these diseases.

Nicholas Megjugorac, Ph.D. * - Stratford - My work is currently focused on three aspects of the IL-17 axis of inflammation. (I) Defining the role of IFN-lambda on Th17 differentiation and cytokine expression. (II) Characterizing differences in IL-17 signaling in normal and malignant prostate cells. (III) Identifying mRNA expression profiles in the whole blood of patients with Inflammatory Bowel Disease. Email: N.Megjugorac@Humigen.org

James H. Millonig, Ph.D. * - Piscataway - The lab is interested in developmental neuroscience, using the mouse as a genetic system. The goal is to apply this research to elucidate the genetic causes of autism, a common human disease.

Joseph Nickels, Ph.D. * - Stratford - Our research uses proteomic/genomic methods and mouse models to understand the biology of diseases, such as cancer initiation and metastasis, cardiovascular disease, and infectious mycoses. Our goal is discovering novel genes that can be used as biomarkers and drug targets, thus allowing us to diagnose and treat these diseases. Email: jnickels@mdlab.com

Harvey Ozer, M.D. * - Newark - Carcinogenesis and Regulation of Cellular Aging. We have been studying human diploid fibroblasts (HF) and introduction of genes from the DNA tumor virus SV40 to understand the mechanism of multi-step carcinogenesis ("transformation") in culture and its effect on bypassing cellular aging and facilitating immortalization.

Lynn S. Ripley, Ph.D. * - Newark - Studies in the lab focus on frameshift mutagenesis mechanisms, especially how enzymes go wrong. Special emphasis is on spontaneous mutations in vitro, in model prokaryotic systems and the mutations responsible for human disease (both germline and somatic).

Zoltan Spolarics, M.D., Ph.D. * - Newark - The project investigates the effects of genetic polymorphisms of metabolic enzymes and cytokines (IL-6, IL-10, IFN-γ) on the immune response. We employ genetically modified mice using experimental models of infection in vivo. We also investigate macrophage and T-cell responses in vitro. The human component of the project investigates the effects of genetic polymorphisms on the immune response in trauma patients. Infection, immunity, T-cells, macrophages, red blood cells, chemokines, polymorphism, flow cytometry, injury, host-response, malaria.

Nancy Walworth, Ph.D. * - Piscataway - Studies on cell cycle checkpoints: signal transduction pathways that control cell cycle progression in response to DNA damage or DNA replication blocks, using the genetically tractable fission yeast, Schizosaccharomyces pombe as a model system. Checkpoint defects are apparent in cells of patients with the cancer-prone genetic disorder ataxia telangiectasia (AT).

Lizhao Wu, Ph.D. * - Newark - We use a combination of molecular, cellular, and genetic approaches to identify key molecules that are important for cancer. Both cell culture systems and mouse models are used to delineate various tumor suppressor/oncogenic pathways in the hematopoietic system, prostate gland, and mammary gland.

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