Sphingolipids are structural components of membranes and also bioactive lipids regulating growth, differentiation, apoptosis, intracellular trafficking and membrane turnover among other cellular processes. We use a combined genetic, molecular and biochemical approach to elucidate physiological functions for these lipids and to understand mechanisms that control sphingolipid homeostasis acharya.

-Usha Acharya, Ph.D.

We study gene regulatory mechanisms controlling the timing of animal development, using the C. elegans model system. Developmental timing regulators in C. elegans include microRNAs that control the stage-specific expression of key transcription factors. We aim to understand the molecular mechanisms of post-transcriptional gene regulation by microRNAs, and how microRNAs function in regulatory networks affecting development and disease.

-Victor Ambros, Ph.D.

Our laboratory investigates protein networks around LIM domain proteins to understand the molecular mechanisms underlying their involvement in transcriptional regulation, nervous system development and pathological processes such as cancer. We use mouse and zebrafish as model systems applying molecular, biochemical and genetic methods.

-Ingolf Bach, Ph.D.

Our laboratory is interested in the molecular mechanisms that control how cells grow and divide. We are using genetics, biochemistry and cell biology, in both yeast and mammalian cells, to study how protein degradation by the ubiquitin proteasome system controls cell cycle and metabolic transitions.

-Jennifer Benanti, Ph.D.

Our laboratory studies the biological mechanisms that control human immune responses to infectious agents and transplanted non-self tissues.  To investigate these mechanisms we are using humanized mouse models that contain functional human immune systems.  The humanized mice are generated using immnodeficient mice, which are engrafted with either human hematopoietic stem cells or with mature human immune cells.  These humanized mouse models allow the direct study of human immunity that is not possible with patients.

-Michael Brehm, Ph.D.

We use Drosophila melanogaster as a model organism to study how cells distinguish between normal and dysfunctional chromosomes. We are particularly interested in how p53-dependent and p53-independent signaling pathways regulate apoptosis in response to DNA damage and unprotected telomeres.

-Michael Brodsky, Ph.D.

Our laboratory studies how leukemia oncogenes alter cellular programs to transform hematopoietic stem and progenitor cells into a leukemia initiating cells. We combine genetic, biochemistry, and molecular biology approaches in transgenic mice and human cells to identify and characterize pathways deregulated by mutations in the members of the CBF gene family that redefine survival, self-renewal, and expansion of pre-leukemic progenitors. Recent efforts use this knowledge to develop high throughput small-molecule screens to identify inhibitors of oncoproteins that may be used as new drugs for improved therapies.

-Lucio H. Castilla Ph.D

Our laboratory is interested in the genetic and molecular mechanisms underlying tumor initiation and maintenance. We focus primarily on melanoma, using genetically-engineered zebrafish models and mammalian cultured cells to identify unique features of cancer cells that can potentially be used for diagnostic, prognostic or therapeutic benefit.

-Craig Ceol, Ph.D.

Our research investigates how the glycoprotein spikes on HIV particles interact with the cell surface receptors and neutralizing antibodies. Our aim is to understand how these envelope spikes vary in different parts of the body allowing HIV to evade neutralization and to transmit to a new person. Understanding these issues will help the design of drugs and vaccines to treat and prevent HIV infection.

-Paul Clapham, Ph.D.

Our laboratory has two main interests. One is the mechanism by which phosphoinositides control signal transduction and membrane trafficking in the endosomal system. The second more recent interest is centered on the question of how cells and organisms sense, generate, utilize and store energy. Energy metabolism is essential to life, and many diseases are associated with altered metabolism, including cancer and diabetes. We hope our research will lead to a better understanding and treatment of human diseases.

-Silvia Corvera, M.D.

Our laboratory group is dedicated to the discovery of molecular mechanisms whereby insulin signaling regulates energy homeostasis. This quest includes RNAi screens, digital imaging and TIRF microscopy, phenotyping mice with gene knockouts and analysis of human adipose tissues. We hope to translate our findings to the prevention and treatment of type 2 diabetes.

-Michael Czech, Ph.D.

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-Roger Davis, Ph.D.

Our laboratory investigates the mechanisms of centrosome function, spindle organization, cell cycle progression/checkpoints, cell separation during cytokinesis and asymmetries generated during mitosis. We are interested in the relationship of these processes to cancer, stem cell self-renewal, cancer stem cells and human aging.

-Stephen Doxsey, Ph.D.

Our lab is focused on the identification of regulatory networks controlling gene expression in stem cells. In particular, we are interested in the roles of chromatin regulators in stem cell self-renewal and differentiation, and we take molecular, genomic, and biochemical approaches to understand these processes.

-Thomas Fazzio, Ph.D.

The laboratory focuses on the late events in human immunodeficiency virus (HIV-1) replication, in particular on an endosomal budding machinery that HIV-1 co-opts to promote its egress from infected cells, and on the molecular mechanism by which the viral accessory protein Nef enhances the intrinsic infectivity of newly assembled virions.

-Heinrich Gottlinger, Ph.D.,M.D.

My lab is interested in the mechanisms that regulate gene expression in eukaryotes, and the role of gene expression in various human disease states. A major emphasis is the use of transcription-based approaches and functional screens to identify new genes and regulatory pathways involved in cancer.

-Michael Green, Ph.D.,M.D.

Our laboratory investigates the pathogenesis of type 1 diabetes, how to prevent it, and how to reverse it through islet transplantation. We use mouse and rat models of type 1 diabetes, and are building mice with human immune systems that permit the direct study of human disease without putting patients at risk.

-Dale Greiner, Ph.D.

We study the molecular basis of growth and how defects in growth regulatory pathways contribute to cancer, metabolic disorders, and aging. In particular we are trying to understand how cells simultaneously sense nutrient availability, energy levels, and growth factors and use this information to control cell metabolism, cell growth, and cell proliferation. Our approach is multidisciplinary and employs genetic, cell biological, and biochemical strategies using mice, stem cells, and established mammalian cell lines.

-David Guertin, Ph.D.

Chromosomes carry the genetic material, and their structural organization is key to regulating and protecting that information. Using cell biology, genetics, and biochemistry in C. elegans we are discovering how proteins that package chromosomes impact processes from gene expression to cell division.

-Kirsten Hagstrom, Ph.D.

We use Drosophila melanogaster, the common fruit fly, as a model to study innate immune response and stem cell regulation in the adult intestinal tract. The intestinal tract of the adult fly is a relatively simple organ formed by a layer of epithelial cells interspersed with stem cells. The intestinal tract frequently faces environmental challenges such as pathogenic chemicals and microbes. We are studying how these pathogens stimulate innate immune response and stem cell division, both of which are essential for the survival of the animal.

-Tony Ip, Ph.D.

We study several different classes of proteins used by eukaryotic cells to deposit histones onto DNA, as well as enzyme complexes that chemically modify chromosome proteins in order to alter DNA accessibility. We study these processes in yeast and human cells, using biochemical, genetic, genomic, and cell biological techniques.

-Paul D. Kaufman, Ph.D.

Our research investigates obesity, diabetes and its complications using elegant metabolic procedures and transgenic mouse models of altered metabolism. Our NIH-funded projects examine the role of inflammation in insulin resistance and cardiovascular diseases. The goal of our research is to understand how obesity causes diabetes and to find its cure.

- Jason Kim, Ph.D.

Crystallographic, biophysical, biochemical, and cell biological approaches are used to investigate mechanisms of membrane trafficking and cell signaling. Defects in these fundamental regulatory mechanisms play critical roles in genetically linked disorders and complex disease states including cancer and diabetes.

-David Lambright, Ph.D.

We are interested in how blood vessel identity is programmed. To investigate this process we take advantage of the zebrafish as a model system. We utilize genetic and molecular approaches to identify genes important for endothelial differentiation, while in vivo time lapse analysis allows us to visualize blood vessels as they form in a live embryo. Since this process is evolutionarily conserved, what we learn about blood vessel formation in the zebrafish will be relevant to human disease.

-Nathan Lawson, Ph.D.

Primary pancreatic and liver cancers are deadly malignancies characterized by the rapid decline of patients after diagnosis. Work in the Lewis lab aims to elucidate the molecules and signaling pathways involved in tumor initiation, tumor progression and metastasis, and response to therapy in these tumors, using genetically engineered mouse models, cultured primary cells, and cancer cell lines.

-Brian Lewis, Ph.D.

Research in the laboratory is focused on understanding viral and host factors that contribute to the establishment of persistent viral infections in humans, including human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), and cytomegalovirus (CMV).

-Katherine Luzuriaga, M.D.

Type 1 Diabetes (T1D) is the result of an autoimmune destruction of insulin producing, pancreatic beta cells. The events leading to the disease have usually occurred long before diagnosis and are based on complex interactions between genes and the environment. The currently available rodent models for T1D can only represent a limited number of patients leaving open the question how many different types of T1D exist. To overcome these difficulties and expand our understanding of T1D and other diseases targeting the immune system we are building in vitro models using human pluripotent stem cells. In those stem cell-based model systems genetic and developmental aspects of the disease can be elucidated. The long-term goal is to recapitulate the disease in a patient-specific manner and to identify novel treatment strategies.

-Rene Maehr, Ph.D.

Our lab uses the nematode worm C. elegans as a model organism to investigate how embryonic cells differentiate and communicate during development. In addition, we are investigating the mechanism of RNA interference, a form of sequence-specific gene silencing triggered by double-stranded RNA.

-Craig Mello, Ph.D.

Our laboratory works at the interface of nanomaterial science and biology to develop oral DNA, siRNA, protein and small molecule delivery technologies based on beta-glucan particles processed into porous hollow microspheres loaded with multi-layered nanostructured payload complexes. We collaborate with many investigators to develop research and translational applications for this delivery technology targeting chronic diseases using gene therapy, RNAi, vaccine and small molecule inhibitor approaches.

-Gary Ostroff, Ph.D.

We are interested in the function of the mammalian primary cilium. These organelles play vital roles in the development of mammals and in the etiology of diseases such as polycystic kidney disease and blindness. Our work combines in vitro cell culture studies with mutant mouse models to understand the role of cilia in controlling kidney architecture and formation of the photoreceptor outer segment.

-Gregory Pazour, Ph.D.

Work in the lab is focused on understanding how chromosome structure influences gene transcription, DNA replication and repair, with special emphasis on identifying and characterizing the cellular machines that control chromosome dynamics. We use a combination of chromatin biochemistry, analytical ultracentrifugation, and yeast molecular genetics.

-Craig Peterson, Ph.D.

Our lab studies the biochemistry of post-transcriptional gene expression, particularly cytoplasmic polyadenylation and translational control. We also examine how these processes influence early animal development, cell division and cellular senescence, and neuronal synaptic plasticity and memory consolidation.

-Joel Richter, Ph.D.

Work in the lab addresses RNA localization and embryonic patterning, the response of mitotic cells to DNA damage, and small RNA function in germline development. Studies combine high resolution imaging, genetic, and molecular approaches in Drosophila and mammalian cultured cell systems.

-William Theurkauf, Ph.D.

Our work in focused on understanding the molecular mechanisms involved in the aging process using a combination of genetics, molecular biology and biochemistry. Our long term goal is to increase the healthspan (the number of active, productive years before the onset of age-associated decline) of individuals; redefining middle age.

-Heidi Tissenbaum, Ph.D.

Using C. elegans and mammalian models, we study how lipid homeostasis is affected by genetics or diet and how transcriptional control of methyl donor supply may affect cellular processes such as epigenetics. We also examine links between metabolism and cellular function potentially contributing to human metabolic disorders.

-Amy Walker, Ph.D.

We aim to understand how regulatory networks control animal development, function, and homeostasis; and how dysfunctional networks affect or cause diseases like diabetes, obesity and cancer. We use a combination of experimental and computational systems biology methods to map, characterize and manipulate regulatory networks, most notably in the nematode C. elegans.

-Marian Walhout, Ph.D.

Our focus in the lab is to dissect the functional roles of nuclear receptor PPARs and their co-regulators in glucose and fatty acid metabolism and metabolic diseases, and to understand their molecular mechanisms of action. A combination of tools, including molecular biology, mouse genetics, physiology and genomics, will be employed.

-Yong-Xu Wang, Ph.D.

An essential and characteristic step in human immunodeficiency virus type-1 (HIV-1) replication is the export of the intron-containing gag-pol and env mRNAs from the nucleus to the cytoplasm. The viral regulatory protein Rev mediates this event, in conjunction with the cellular nuclear export machinery and several protein cofactors. Our long-term objective is to gain a detailed understanding of the cellular factors and molecular mechanisms involved in Rev-directed nuclear export, cytoplasmic localization, and function of HIV-1 RNAs.

-Maria Zapp, Ph.D.