Amanda Garner, Ph.D.
Amanda L. Garner is an Assistant Professor in the Department of Medicinal Chemistry, College of Pharmacy at the University of Michigan. She is also affiliated with the University of Michigan Program in Chemical Biology, Translational Oncology Program and Center for RNA Biomedicine. She received her Ph.D. in Chemistry in 2008 from the University of Pittsburgh working under the supervision of Professor Kazunori Koide in the areas of fluorescent chemosensors and solid-phase organic synthesis. She then completed NIH-funded postdoctoral studies in the laboratory of Professor Kim Janda at The Scripps Research Institute in La Jolla, California working in the area of chemical biology. Dr. Garner’s independent research integrates chemical biology, medicinal chemistry and molecular and cellular biology approaches for studying cap-dependent mRNA translation and microRNA-mediated gene regulation. In particular, her laboratory is focused on the development of conceptually new high-throughput screening assays for the identification of chemical probes. The anticipated outcome of these studies is the validation of mRNA translation-related targets for future drug discovery efforts and the betterment of human health.
Jayakrishnan Nandakumar, Ph.D.
Nandakumar Lab utilizes a combination of biochemistry, structural biology, and cell biology to understand the molecular basis for end protection of human chromosome ends by the shelterin complex, and end replication by the ribonuclear protein enzyme telomerase. I started as an assistant professor at University of Michigan in Fall of 2013 and brought with myself extensive expertise in biochemistry, X-ray crystallography and human cell biology. Our group recently described how a mutation in the gene coding for TPP1 results in the telomerase deficiency disease, dyskeratosis congenita (Kocak et al). These studies were inspired by my postdoctoral efforts that discovered a surface in TPP1 called the TEL patch, which binds telomerase to recruit it to its site of action in the cell and facilitates telomere elongation. While our efforts on the TEL patch highlight our interest in end replication, my postdoctoral studies also interrogated in depth the role of TPP1, and its binding partner, POT1, in end protection. As part of my graduate studies I solved several crystal structures of RNA and DNA ligases bound to their ‘broken’ RNA/DNA substrates to illustrate how these two families of repair enzymes use distinct strategies for joining RNA versus DNA ends. Most recently, we have come across a novel form of gene regulation that involves an intragenic noncoding RNA, which differentially influences the fates of isoforms of a telomeric gene.
Muneesh Tewari, Ph.D.
Dr. Tewari earned an M.D. and Ph.D. from the University of Michigan in 1997, where he worked with Dr. Vishva Dixit on mechanisms of apoptosis for his thesis research. He then completed an internship and residency in Internal Medicine at the University of Michigan Hospitals and a Medical Oncology clinical fellowship at Dana-Farber Cancer Institute. He subsequently trained in systems biology and genetics at Dana-Farber Cancer Institute/Harvard Medical School, as a postdoctoral fellow bridging the labs of Dr. Marc Vidal and Dr. Gary Ruvkun. Dr. Tewari joined the faculty of Fred Hutchinson Cancer Research Center in 2005 where he began an independent research program studying microRNAs and cancer.
In 2008, Dr. Tewari’s laboratory reported that microRNAs are released from cancer cells into the bloodstream where they circulate in a highly stable form. This has led to burgeoning interest in circulating microRNAs as biomarkers for cancer and other diseases. His laboratory has gone on to study the biochemistry of extracellular microRNAs (including mechanisms that stabilize them in the extracellular environment), to develop fundamental understanding pertinent to developing microRNA-based disease biomarker approaches, and to advance methodology for highly sensitive and reproducible measurement of extracellular microRNAs. He also currently leads an NIH-funded U01 team focused on performing discovery and establishing reference profiles of extracellular RNAs using next generation sequencing methods.
In the course of this research, Dr. Tewari has become inspired to develop a next generation of biomarker approaches for human health and disease that will involve serial monitoring at high time resolution at drastically lower cost than is currently possible. This will require both fundamental research on biomarkers and their relationship to physiology, as well as technology development grounded in advances in engineering and the physical sciences. In 2014, Dr. Tewari moved to the University of Michigan, where he is pursuing this inspiration as a tenured faculty member in the Departments of Internal Medicine and Biomedical Engineering, in the Center for Computational Medicine and Bioinformatics, and in the inter-disciplinary Biointerfaces Institute.
Peter Freddolino, Ph.D.
The regulatory networks of bacteria play a key role in their information processing capabilities, coordinating and executing interactions with their environments. Quantitative, predictive models of these networks would be tremendously beneficial for facilitating the development of new antimicrobial therapies, enabling synthetic biology applications, and understanding bacterial evolution and ecology. Ultimately, the aim of my laboratory is to build a multiscale framework enabling modeling of bacterial regulatory networks at any level of detail, from atomistic to cellular. To this end, we develop and apply high-throughput experimental methods for measuring biomolecular interactions and cellular regulatory states in vivo, and for profiling the phenotypic consequences of regulatory changes. In tandem with these experimental approaches, we use molecular simulation and mathematical modeling to obtain high-resolution insight into the biomolecular interactions driving regulatory networks, and the systems-level effects of altering them.
More detailed information, and publication lists, are available on the Freddolino lab website.
Peter Todd, Ph.D.
Peter Todd, M.D., Ph.D. is the Bucky and Patti Harris professor of neurology in the University of Michigan Medical School and a staff physician at the Ann Arbor VA Medical Center. Dr. Todd graduated from the University of California, San Diego and obtained his medical and doctoral degrees at the University of Wisconsin. He completed a medical internship and residency in neurology at the Hospital of the University of Pennsylvania, and a research intensive fellowship in movement disorders and neurogenetics at the University of Michigan. Dr. Todd’s research targets the mechanisms by which RNA and RNA processing contribute to neurodegenerative disorders, with a specific interest in Fragile X-associated tremor ataxia syndrome (FXTAS). For his work on FXTAS pathogenesis, he received the 2014 Hagerman Prize from the National Fragile X Foundation. Dr. Todd serves as co-director of the Fragile X clinic at the University of Michigan where he sees adult patients with FXTAS, Fragile X Syndrome, and other Fragile X-associated Disorders.
Stephen C.J. Parker, Ph.D.
The Parker Lab at the University of Michigan is part of the Departments of Computational Medicine & Bioinformatics and Human Genetics, and is affiliated with the Genome Science Training Program at the Center for Statistical Genetics and the Center for RNA Biomedicine.
Our research group uses an integrative approach in the general fields of computational biology and functional genomics. The major goal of the lab is to generate mechanistic knowledge about how disease susceptibility is encoded in the non-coding portion of the genome, with a focus on type 2 diabetes.
Sundeep Kalantry Ph.D.
The focus of Kalantry laboratory is to understand how X-chromosome inactivation occurs. X-inactivation equalizes X-linked gene expression between male and female mammals by transcriptionally inactivating one of the two X-chromosomes in females. X-inactivation is required for the viability of female cells and is a paradigm of epigenetic inheritance, given that within a shared nucleoplasm one X-chromosome of an identical pair becomes inactivated while the other remains active and that replicated copies of the inactive and active X-chromosomes faithfully maintain their transcriptional states across many cell division cycles. X-inactivation is controlled by long non-coding RNAs and chromatin/transcription regulators, both of which are a focus of our lab.