Subhasis, B. Biswas, Ph.D. * - Stratford - Our laboratory is interested in dissecting the mechanisms of DNA replication in prokaryotic and eukaryotic systems with goals of developing novel anti-microbials and anti-proliferation drugs. Email: email@example.com
Kenneth J. Breslauer, Ph.D. * - Piscataway - Characterization of the molecular interactions that control biopolymer structure and stability, drug-binding affinity and specificity, relating biophysical properties to biological function, correlating structure and energetics.
Steven Brill, Ph.D. * - Piscataway - Research in the laboratory focuses on cellular mechanisms that control genome stability. We use genetics and biochemistry to identify and characterize enzymes involved in DNA replication, DNA repair and DNA recombination using yeast as a model system.
Salvatore J. Caradonna, Ph.D. * - Stratford - My laboratory is interested in the post-translational mechanisms that regulate proteins involved in base-excision repair of DNA. We are studying the aberrant pathways that lead to uracil misincorporation into DNA and strategies that may exploit these pathways for cancer drug development. We are also involved in the study of atypical cyclin-like proteins that affect cell-cycle phase transitions. Email: firstname.lastname@example.org
Frederick D. Coffman, Ph.D. * - Newark - Proteins and DNA sequences which regulate the initiation of DNA replication at human replication origins. We also examine the mechanism of tumor necrosis factor cytotoxicity and modulation of TNF sensitivity by antitumor drugs.
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.
Abram Gabriel, M.D. * - Piscataway - My laboratory focuses on the study of mechanisms and consequences of retrotransposon reverse transcription.
Utz Herbig, Ph.D * - Newark - Our laboratory is interested in understanding how telomeres contribute cellular senescence in mammalian cells. As cellular senescence is a critical tumor suppressing mechanism, but also is thought to contribute to organismal aging, our studies are relevant for both aging- and cancer-research.
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.
Andreas Ivessa, Ph.D. * - Newark - My laboratory is interested in the mechanisms how mitochondrial DNA is replicated, and how damage during replication is recognized and repaired. In particular we study several DNA helicases that are involved in these processes using budding yeast as a model system.
David Kaback, Ph.D. * - Newark - Chromosome structure and function in yeast Meiotic chromosome pairing and segregation Control of meiotic recombination and chiasma interference.
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.
Stuart G. Lutzker, M.D., Ph.D. * - Piscataway - My lab examines the role of the p53 transcription factor in the cellular response to DNA damage. We have developed a unique genetic system to test the role of specific post-translational modifications in fine-tuning the p53 response.
Kiran Madura, Ph.D. * - Piscataway - Ubiquitin-mediated protein degradation in DNA repair and signal transduction.
Kim S. McKim, Ph.D. * - Piscataway - My laboratory is characterizing genes with important roles in either meiotic recombination or segregation of chromosomes using Drosophila melanogaster as a model system. Many of these genes are also involved in DNA repair and we are characterizing their functions during Drosophila development.
Joachim Messing, Ph.D. * - Piscataway - We work on two genomics projects. We sequence orthologous regions of the maize and sorghum genomes to study their synteny and the four fold expansion of the maize genome. We also participate in the international effort to sequence the rice genome. Further information on our research can be found at Dr. Messing`s home page.
Mukund J. Modak, Ph.D. * - Newark - Molecular mechanism of DNA synthesis: We are investigating the mechanisms of enzymatic DNA replication. DNA polymerases from bacterial, tumor viral and mammalian sources are included in these studies. Each enzyme study also offers an opportunity to probe in vivo implication of its unique properties.
Susan Muller-Weeks, Ph.D. * - Stratford - Research in the laboratory focuses on the repair of uracil in DNA, which is critical for the maintenance of genomic integrity. Specifically we are elucidating transcriptional and post-translational pathways that regulate expression of uracil-DNA glycosylase under normal cellular conditions and in response to anti-tumor agents. Email: email@example.com
Carol S. Newlon, Ph.D. * - Newark - Studies on the mechanism of eukaryotic chromosome replication, using the budding yeasts, Saccharomyces cerevisiae and Cryptococcus neoformans, as model systems. Our current focus is on the structure and regulation of chromosomal DNA replication origins.
Lyndi Rice, Ph.D. * - Stratford - The focus of our group is to elucidate the molecular regulation of several tumor suppressors and oncogenes in the onset of gynecological cancers, using cell culture, primary tissues, and mouse model systems. Through our research, we will identify novel biomarkers to aid in early detection and potential drug targets that modulate tumor progression. Email: firstname.lastname@example.org
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).
Katsunori Sugimoto, Ph.D. * - Newark - Our research focuses on molecular mechanisms of how cells activate "checkpoint" signaling pathways after DNA damage. Checkpoint defects are associated with cancer-prone genetic disorder ataxia telangiectasia (AT).
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).