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We are combining top-down and bottom-up approaches to synthetic biology; we use tools of protein engineering and molecular biology, together with novel synthetic cell technologies, to understand and modulate biological processes in complex systems. |
612-625-9066 |
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We study the genetics of complex traits: how variation in genome sequences influences individual molecular, cellular and organismal features. We also seek to understand the evolutionary forces that shape genomic diversity. |
612-301-1243 |
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T2D is the most common chronic disease affecting human health, affecting more than 347 million individuals worldwide. T2D is a complex disease characterized by pancreatic β-cell failure to make sufficient amounts of insulin in the setting of obesity and insulin resistance in peripheral tissues. The risk for T2D is determined by many factors. Our genetic makeup can predispose us for T2D, and lifestyle can also reduce or exacerbate health risks. But in recent years, our studies and those of others have shown the importance of babies' time in the womb for influencing health over our lifespan. We and others have shown that poor uterine environments can increase the risk of many diseases in adulthood, including diabetes. Therefore, the long-term goal of the Alejandro Lab is to stop the vicious cycle of diabetes by launching a two-pronged research program for both intervention and prevention of this disease:
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612-625-5149 |
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| Transplant immune responses/therapy and use of induced pluripotent stem cells |
612-626-2734 |
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We investigate mechanisms that coordinate cell behaviors across great distances during tissue morphogenesis. |
612-301-2474 |
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Cell adhesion, signal transduction, cytoskeleton, and C. elegans. |
612-625-1299 |
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Yeast and Human Cell Cycle Control |
612-624-3442 |
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Clathrin-mediated endocytosis; mammalian intracellular membrane trafficking. |
612-625-3707 |
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Structure, assembly and dynamics of actin-based cytoskeletal network |
612-624-3195 |
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| C. albicans genetics and pathogenesis |
612-624-1912 |
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| Focuses on the role of the androgen receptor (AR) and alterations in AR signaling in prostate cancer development and progression |
612-625-1504 |
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| Dong, Xiao |
We focus on testing the mutation theory of aging: if accumulation of DNA mutations in normal somatic cells is a causal mechanism to age-related functional decline. We approach this by developing and applying state-of-the-art single-cell multi-omics technologies and machine learning algorithms. |
612-626-7090 |
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The research in the Engelhart laboratory is directed towards better understanding nucleic acid folding and function in order to advance two broad themes: 1) the development of novel nucleic acid-based imaging, analytical, and diagnostic technologies and 2) the elucidation of unanticipated roles for nucleic acids in vivo. |
612-625-1950 |
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Molecular Basis of Muscular Dystrophy; Role of Actin in Cell Polarity |
612-626-6517 |
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Signal transduction and lymphocyte development |
612-625-0401 |
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Cytoskeleton and Cell Motility, developmental mechanisms, neuroscience, and regulation of gene expression |
612-625-6158 |
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Chromatin mechanics and dynamics; Quantitative fluorescence microscopy |
612-626-6760 |
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Regenerative medicine, cardiogenesis, and stem-cell biology. |
612-625-8988 |
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| Gill, Matthew |
We are interested in discovering novel signaling pathways and mechanisms that affect development and aging in the nematode Caenorhabditis elegans using a combination of genetic, drug screening and biochemical approaches. |
612-301-6314 |
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Fundamental and fascinating developmental processes of meiosis and fertilization using C. elegans |
612-624-3955 |
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Transposons, human gene therapy, vertebrate gene expression, mouse, zebrafish |
612-624-6736 |
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How Rb/E2F1 mediated apoptosis is regulated in normal and cancer cells |
612-626-2905 |
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Cytoskeleton and cell motility, developmental mechanisms |
612-626-2949 |
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Molecular mechanism of cell-fate determination in T cells |
612-625-1616 |
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Kidney development, transcriptional regulation, microRNAs, primary cilia, polycystic kidney disease (PKD) |
612-625-3654 |
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Development, homeostasis and trafficking of T lymphocytes |
612-625-1496 |
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| Junge, Harald | Retina, neurovascular interactions, wnt signaling |
612-624-6017 |
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Understanding the molecular and genetic mechanisms of vertebrate limb development and apply the study to elucidate the mechanisms of congenital limb in human and limb regeneration |
612-626-9935 |
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Nuclear reprogramming in somatic cell nuclear cloning and stem cells |
612-624-0498 |
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The role of DNA repair and recombination in maintaining genome stability |
612-624-9244 |
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Cell cycle regulation, Ubiquitination and proteolysis, Genetic mechanisms of tumorigenesis |
612-624-4201 |
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| Genome engineering, pioneering full gene and gene cluster replacement technologies; modeling the genetics of human disease in the mouse; molecular mechanism underlying Alzheimer’s Disease and Related Dementias, with a current focus on the phospho-dynamics of TAU |
612-626-4521 |
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Stem Cell Biology: regulatory pathways, diseases and therapies Transcriptional control of mesoderm development |
612-626-5869 |
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The Lange lab studies how steroid hormone receptor (SR) positive and hormone-influenced cancers escape molecular targeted therapies. Signal transduction is an essential role of SRs. Indeed, all SRs can rapidly activate cytoplasmic protein kinases and act as “growth factor sensors”. In this role, SRs are heavily phosphorylated by mitogenic protein kinases (MAPKs, AKT, CDKs) that are frequently elevated and activated in SR+ (breast and reproductive tract) cancers. Phosphorylation of SRs alters their binding partners and promoter selection and influences cancer cell fate/plasticity by regulating genes that specify proliferative, pro-survival, metabolic, and cancer stem cell programs. Identifying the required kinases and co-activator partners of phospho-SRs will enable the targeting of multiple signaling molecules in addition to SRs, which is predicted to halt cancer metastasis, prevent recurrence, and increase patient survival. |
612-626-0621 |
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Identification and understanding of genes involved in cancer development |
612-626-4979 |
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The translational development of therapies for treating neurological disorders. |
612-626-9203 |
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Focus on signaling and transcriptional mechanisms that regulate osteoclast differentiation |
612-626-5582 |
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Cell and molecular biology of HIV and HTLV |
612-626-5525 |
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Gene therapy for genetic disease and cancer using viral and non-viral vectors |
612-626-1497 |
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Craniofacial muscles in health and disease |
612-626-0777 |
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Integrative systems biology of cardiovascular function; Cardiac gene therapy; Transgenic models of heart disease; Molecular mechanisms of sarcomere function; Human iPS cell cardiac myocytes |
612-625-8296 |
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My lab works on pediatric cancer genetics, immunotherapy, and gene therapy using cutting edge technologies, including DNA transposons, TALENs, and CRISPR/Cas9. |
612-625-2226 |
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Computational biology and functional genomics - Machine learning for integrating diverse genomic data to make inferences about biological networks |
612-624-8306 |
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| Nakagawa, Yasushi | Mammalian brain development, cell type specification and establishment of neuronal connectivity |
612-626-4916 |
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Molecular and genetic analysis of Drosophila development |
612-625-1727 |
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Developmental control of growth and cell proliferation in Drosophila |
612-625-5158 |
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Cell-cell interactions in growth, differentiation, and development |
612-626-0642 |
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Mechanisms controlling lineage decision and reprogramming, and application to regenerative medicine |
612-625-4984 |
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Regulation of dynein-based motility |
612-626-1901 |
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| Rivera-Mulia, Juan Carlos | Research in the Rivera-Mulia lab focuses on understanding how DNA replication timing and large-scale chromosome organization are regulated and maintained in distinct cell types and remodeled during development as well as how alterations in nuclear architecture disrupt gene function in human disease. | riveramj@umn.edu |
| Rougvie, Ann | Developmental timing in C. elegans: from microRNAs to nutritional cues |
612-624-4708 |
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Our group invents and applies protein engineering technologies to study fundamental functional principles of natural and artificial living systems at a cellular level. |
612-625-1180 |
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| Selmecki, Anna | We employ diverse yeast model systems (Saccharomyces cerevisiae, Candida albicans, Candida auris, etc.) to understand how genome instability contributes to adaptation (eg. antifungal drug resistance) and determine the underlying mechanisms that promote genome instability. | selmecki@umn.edu |
| Shima, Naoko | Uses the laboratory mouse as a model to understand a causative link between chromosome instability and cancer |
612-626-7830 |
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Lymphocyte and tumor cell adhesion, migration and signal transduction |
612-626-6849 |
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Protein acrobatics - Study of protein function via protein engineering; Focus on cell signaling and motor proteins |
612-301-1537 |
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| Skubitz, Amy | Discovery and validation of biomarkers for ovarian cancer |
612-625-5920 |
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My laboratory is interested in understanding the lifecycle of retroviruses and use this information 1) to identify new drug targets for HIV, 2) to develop better vectors for gene therapy and 3) to use these vectors for gene discovery. |
612-625-6988 |
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My research focuses mainly on the roles of microRNAs in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), obesity, insulin resistance and liver cancer, with the goal to develop novel therapeutic approaches for these disorders. |
612-624-9961 |
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Understanding the genetics of cancer in order to develop individualized, targeted therapies |
612-626-6971 |
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| Steer, Clifford | Non-viral gene therapy using nanocapsules and the Sleeping Beauty (SB) transposon; antiapoptosis of neurodegenerative disorders using ursodeoxycholic acid as a therapeutic drug; genomic methylation changes associated with transposition of SB; and induced by microRNAs |
612-625-8999 |
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Molecular genetic analysis of unconventional myosin function |
612-625-8498 |
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Stem cell gene therapy |
612-626-4949 |
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Role of cardiac progenitor cells in vivo during cardiac development |
612-626-1853 |
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| Venteicher, Andrew | We seek to map the developmental origins of chordoma 1) to understand the epigenetic requirements that are necessary for malignant transformation in these challenging tumors, 2) to provide a framework to explain the variability in clinical behavior of chordoma, and 3) delineate vulnerabilities that may be used as new therapeutic targets. We use a variety of epigenomics, single cell genomics, and biochemistry approaches to study the connection between notochordal development and human chordoma tumors. | aventeic@umn.edu |
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Plant genome engineering through homologous recombination; Retrotransposable elements and genome organization |
612-626-4509 |
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Evaluate retroviral-mediated gene transfer in hematopoietic cells and reversal of the disease process in vitro thus providing the impetus to initiate clinical trials of gene therapy |
612-625-7422 |
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Cancer gene-therapy and virotherapy |
612-624-9131 |