Usha Acharya, Ph.D.
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.
Ingolf Bach, 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.
Jennifer Benanti, 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.
Michael Brehm, 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 Brodsky, 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.
Lucio H. Castilla 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.
Paul Clapham, 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.
Silvia Corvera, M.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.
Michael Czech, Ph.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.
Roger Davis, Ph.D.
The cJun NH2-terminal kinase (JNK) signal transduction pathway is implicated in several stress-related disease processes including cancer, diabetes, inflammation, and stroke. Our hope is that drugs targeting the JNK pathway may be useful for the treatment of these diseases. The goal of this laboratory is to understand the molecular processes that are engaged by JNK in both health and disease.
Stephen Doxsey, 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.
Thomas Fazzio, 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.
Research in this lab is concerned with the both the development and the application of light microscopy and imaging in cell biology and biophysics. Some driving problems include imaging the molecular components driving endocytosis and exocytosis/secretion in various cell types, and the imaging of intracellular calcium signaling in excitable cells such as smooth muscle cells, chromaffin cells, and neurons.
Manuel Garber, PhD, associate professor of molecular medicine and bioinformatics and integrative biology, and director of the Bioinformatics Core. Dr. Garber’s methods have been critical to the discovery and characterization of a novel set of large intergenic non-coding RNAs (lincRNAs) and to our understanding of the immune transcriptional response to pathogens. In September 2012, Dr. Garber moved to the University of Massachusetts Medical School to establish his laboratory and direct the Bioinformatics core.
Heinrich Gottlinger, Ph.D.,M.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.
Michael Green, 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.
Dale Greiner, Ph.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.
David Guertin, 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.
Tony Ip, 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.
Paul D. Kaufman, 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.
Anastasia Khvorova, Ph.D.
Develop and characterize novel RNA chemistries to promote efficient oligonucleotide internalization and tissue distribution.
Jason Kim, 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.
David Lambright, 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.
Nathan Lawson, 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.
Michael Lee, Ph.D.
Treatment of many human diseases, including cancer, typically involves modulation of signal transduction pathways. These pathways are functionally integrated, very plastic, and incredibly sensitive to environmental context. Our group uses a combination of experimental and computational approaches to study the organization and function of signaling networks controlling the growth, survival, and death of cancer cells. We are particularly interested in understanding the adaptive properties that cells engage when faced with anti-cancer drugs, as well as identifying genetic, non-genetic, and contextual factors that contribute to the therapeutic variability seen in cancer patients.
Brian Lewis, 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.
Distinguished physician–scientist Jeremy Luban, MD has been appointed professor of molecular medicine at UMass Medical School and the David L. Freelander Memorial Professor in HIV/AIDS Research. Dr. Luban’s research focuses on understanding host cell factors that contribute to HIV viral replication. He has identified Cyclophilin A and Trim 5 among more than thirty HIV-1 regulatory host factors. His work will contribute to the development of drugs and vaccines targeting HIV virus infections and other disease states. NIH/NIDA named him a 2012 Avant-Garde Awardee for HIV/AIDS research.
Katherine Luzuriaga, M.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).
Craig Mello, 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.
Gary Ostroff, 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.
Gregory Pazour, 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.
Joel Richter, 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.
Caterina Strambio De Castillia grew up in Italy and received her Laurea in Biologia (equivalent to B.S./M.S.) from the University of Pavia in 1988. She obtained her Ph.D. (1992-1998) working with Gunter Blobel at The Rockefeller Universitycore. Her work has been supported by the American Cancer Society, the European Union and the Swiss National Science Foundation. In 2012, Dr. Strambio De Castillia joined the Program in Molecular Medicine at the University of Massachusetts Medical School.
William Theurkauf, 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.
Heidi Tissenbaum, 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.
Our research interests are focused on understanding how aneuploidy affects cellular physiology and metabolism, and how aneuploidy influences cell evolution leading to further gross genomic alterations. Utilizing Saccharomyces cerevisiae as a model organism, we generated a series of aneuploid strains, each carrying an additional copy of 1 of the 16 yeast chromosomes and characterized their effects on cell physiology.
Amy Walker, 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.
Marian Walhout, 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.
Yong-Xu Wang, 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.
Maria Zapp, 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.
From: Martin, Gene Sent: Monday, December 23, 2013 2:42 PM To: Martin, Gene Subject: Anast