Faculty Research Interests
John Abrams, Ph.D.
Our lab applies genetic systems to explore how pivotal tumor suppressors function to control stem cell biology.
Michalis Agathocleous, Ph.D.
We study how metabolites regulate hematopoietic stem cell function, and how the metabolism of cancer cells compares to the metabolism of the normal stem cells that give rise to cancers. We are using a combination of mouse genetics, metabolomics, and stem cell biology approaches to investigate the function of metabolic pathways in stem cells and cancers in vivo.
Laura Banaszynski, Ph.D.
Our long-term goal is to determine how chromatin influences developmental cell-fate decisions. We take the view that chromatin acts as both a platform for the integration of signaling information received from local cellular environments, as well as a regulator of gene expression changes required for cellular response to those signals. We use a combination of molecular biology, biochemistry, and genomics to study these questions in the context of preimplantation development, embryonic and adult stem cell biology, and cancer.
Rhonda Bassel-Duby, Ph.D.
We are interested in understanding the molecular mechanisms that regulate striated muscle (skeletal muscle and heart) during regeneration in response to injury and disease. We study molecular factors that control satellite cells, which are skeletal muscle stem cells. We are also defining factors involved in reprogramming fibroblasts to cardiac cells to repair the heart after injury.
Michael Buszczak, Ph.D.
We seek to understand how mRNA translation and chromatin organization help to maintain the balance between stem cell self-renewal and differentiation in vivo.
Thomas Carroll, Ph.D.
The Carroll lab is interested in the mechanisms underlying stem cell renewal and differentiation in the kidney. Much of our research focuses on how the ultimate fate of progenitor cells is affected by their microenvironment.
Elizabeth Chen, Ph.D.
My laboratory is interested in discovering the overarching principles of cell-cell fusion in development and regeneration. We use genetics, biochemistry, cell biology, and biophysics to understand the functions of genes required for cell-cell fusion in organisms ranging from insects to mammals. We aim to achieve a mechanistic understanding of cell-cell fusion and eventually modulate this process in stem cell-based therapy for muscle degenerative diseases.
Ondine Cleaver, Ph.D.
Our lab aims to elucidate the molecular events required for cells to proliferate and take on their specialized functions within tissues such as the pancreas and blood vessels. Understanding these principles will help us to characterize genes that may be required to reactivate these processes during tissue regeneration, as well as to identify molecular lesions that underlie human birth defects and disease.
Jim Collins, Ph.D.
Schistosomes are parasitic flatworms that cause significant disease and disability in more than 200 million of the world’s poorest people. Using a variety of functional genomic approaches we seek to understand fundamental aspects of schistosome biology, including the biology of somatic and reproductive stem cells.
Maralice Conacci-Sorrell, Ph.D.
Our lab employs mouse models, metabolomics, and molecular biology approaches to study transcriptional networks that control cellular fitness during embryonic development and cancer.
Michael Dellinger, Ph.D.
Gorham-Stout Syndrome is a rare disease characterized by the presence of lymphatic vessels in bone and by the disappearance of affected bones. The Dellinger lab is investigating the molecular mechanisms driving the degeneration of bone in Gorham-Stout Syndrome and is working toward identifying therapies to promote the regeneration of bone in this disease. The Dellinger lab is also investigating approaches to promote the repair of damaged lymphatic vessels as a way to treat lymphedema, a common complication in cancer survivors.
Peter Douglas, Ph.D.
Our laboratory is interested in understanding how tissues such as the nervous system respond to traumatic injury. Using high-throughput screening in the nematode C. elegans in combination with murine models, we seek to uncover the short and long-term regenerative capacity for stress response and protein homeostasis pathways in brain injury.
Steven Gray, Ph.D.
My lab focuses on AAV vector development tailored to serve specific clinical and research applications involving the nervous system. We develop novel AAV capsids amenable to widespread CNS gene transfer.
Fred Grinnell, Ph.D.
Research in my laboratory focuses on the biomechanics of connective tissue repair and the pathobiological features that influence healing of human burn and chronic skin wounds. My studies concern not only the research itself, but also the nature of scientific practice underlying research and the bioethical challenges of carrying out research with humans.
Robert Hammer, Ph.D.
We are involved in mouse embryonic stem cell biology and genetic manipulation of the rodent genome.
Joseph Hill, M.D., Ph.D.
Dr. Hill’s research group strives to decipher mechanisms of structural, functional, and electrical remodeling in heart disease with an eye toward therapeutic intervention. Our work is disease-oriented, focusing on load-induced ventricular hypertrophy, ischemia/reperfusion injury, and diabetic cardiomyopathy. Specific areas of emphasis include HDAC-dependent control of cardiac plasticity, cardiomyocyte autophagy, metabolism, and FoxO-driven transcriptional events.
Gary Hon, Ph.D.
We are fascinated by the complexity of gene regulation in mammalian cells, and we seek to understand and control this complexity for therapeutic genome engineering. By integrating tools at the interface of genomics, bioinformatics, and biotechnology, we are developing new approaches for high-throughput and systematic cellular engineering.
Jenna Jewell, Ph.D.
The Jewell laboratory investigates the molecular mechanisms by which cells sense nutrients, such as amino acids, through the mammalian target of rapamycin complex 1 (mTORC1). We are interested in understanding how nutrients regulate mTORC1 signaling in cancer and metabolic diseases, as well as stem cell function.
Jin Jiang, Ph.D.
The Jiang lab studies cell signaling mechanisms that control embryonic development and adult tissue homeostasis. We are particularly interested in Hedgehog, Hippo, and BMP signaling pathways and their roles in the regulation of intestinal stem cell activity during tissue homeostasis and regeneration.
Jane Johnson, Ph.D.
The Johnson Lab focuses on the function of neural specific transcription factors to probe mechanisms that control the balance of neural progenitor cell maintenance and differentiation, and the generation of neuronal diversity, particularly in the spinal cord. Her group also uses the same factors to study the generation of neural cancers such as glioblastoma and neuroendocrine lung carcinoma.
Helmut Krämer, Ph.D.
Our lab uses genetic and cell biological approaches in Drosophila to analyze the molecular pathways that regulate cellular stress responses. We are especially interested in autophagy and the unfolded protein response, their regulation in developing tissues, and their roles in maintaining neuronal health.
Lu Q. Le, M.D., Ph.D.
The Le laboratory focuses on the cellular mechanisms that regulate neural-crest derived tissue development, regeneration and tumorigenesis, specifically the biology of neurofibromatosis as well as hair pigmentation and development.
Benjamin Levi, M.D.
We study how tissue resident mesenchymal precursor cells respond to injury and undergo fate change as a response to the inflammatory response. We are interested in the interaction between immune cells, the extracellular matrix and tissue resident mesenchymal cells. Using single cell technologies and lineage specific deletion models, we seek to identify central pathways and translate these findings by identifying druggable targets.
Ning Liu, Ph.D.
We are interested in the mechanism of heart repair and regeneration after myocardial injury. We study the functions of a unique population of cardiac progenitor cells in cardiac regeneration under normal and diseased conditions. Understanding the mechanisms of cardiac regeneration is an essential step toward improving the regenerative capacity of the adult heart.
Raymond MacDonald, Ph.D.
Our interests are the molecular mechanisms that specify and maintain cell-type identity, explain the plasticity of cellular identity in adulthood, and may be manipulated for tissue regeneration.
Pradeep Mammen, M.D.
The Mammen Laboratory seeks to investigate how alterations in the metabolic and redox states of myogenic progenitor cells can modulate the proliferative and differentiative capacities of these cells. Ultimately, the ability to selectively regulate the metabolic and redox states of cardiac and myogenic progenitor cells may provide opportunities for the development of novel therapeutic approaches for the treatment of patients with advanced heart failure and/or muscular dystrophy.
Denise Marciano, M.D., Ph.D.
The Marciano lab is interested in elucidating how nephron progenitor cells transition to form epithelial tubules in the developing kidney. We are also studying how progenitor cells form the renal glomerulus, the filtration unit of the kidney. We are using both mouse genetics and cell biology to understand the functions of various proteins required for these processes.
Joshua Mendell, M.D., Ph.D.
The Mendell laboratory investigates the regulation and functions of microRNAs and other noncoding RNAs in mammals. We are particularly interested in the roles of these transcripts in normal physiologic processes, including wound healing and tissue regeneration, and in diseases such as cancer.
Carole Mendelson, Ph.D.
Our research is focused, in part, on genetic and epigenetic mechanisms underlying fetal lung development, alveolar epithelial type II cell (AEC2) differentiation and surfactant synthesis. Our recent studies involve regulation of the capacity of AEC2 cells to produce immune modulators, which shield the alveolar epithelium from oxidative and inflammatory stress, and protect against development of lung fibrosis and cancer.
Sean Morrison, Ph.D.
My lab studies the mechanisms that regulate stem cell self-renewal in the hematopoietic and nervous systems and the ways in which those mechanisms are hijacked by developmentally related cancers to enable neoplastic proliferation.
Ping Mu, Ph.D.
Two of the biggest challenges in treating advanced prostate cancer are varying responses and acquired resistance to antiandrogen therapy. We seek to understand the mechanisms of antiandrogen resistance, to identify novel biomarkers, and to develop therapeutic approaches to prevent or overcome resistance.
Nikhil Munshi, M.D., Ph.D.
Our lab seeks to understand the molecular mechanisms by which lineage commitment is achieved in the cardiac conduction system. We believe that such fundamental insight will guide future efforts to regenerate the conduction system and restore normal cardiac rhythm in patients suffering from arrhythmias.
Kathryn O’Donnell, Ph.D.
The O’Donnell laboratory is focused on understanding the mechanisms that contribute to tumor initiation, progression, and metastasis. We have identified novel genes that promote liver cancer, leukemia, and non-small cell lung cancer. Currently, we are investigating the regulation and function of cell surface receptors in lung cancer using molecular and biochemical studies, and animal models. These studies may provide new therapeutic approaches to target cancer cells.
Kim Orth, Ph.D.
Dysregulation of the UPR is a major contributor in tissue degeneration and aging, thus identifying the mechanisms that regulate the UPR may lead to the development of new therapies for degenerative diseases. Our lab uncovered a unique mechanism by which a master regulator of the UPR is regulated by AMPylation and deAMPylation in response to ER stress. These activities have been implicated in tissue regeneration after chronic stress and our interest are to understand the role of AMPylation in degeneration/regeneration using various animal models.
Duojia (DJ) Pan, Ph.D.
The Pan laboratory uses Drosophila and mice as model systems to elucidate the general mechanisms underlying organ size control in animals and the way these mechanisms regulate tissue homeostasis in normal and pathological conditions.
James Richardson, D.V.M., Ph.D.
My lab studies the pathology of genetically engineered mice from prenatal stages to late adulthood.
Ben Sabari, Ph.D.
Our primary goal is to understand how the billions of molecules within the nucleus are organized into condensates to carry out gene activation in normal and diseased cell states. We study how nuclear condensates form at specific genomic loci, how they function once formed, and how they are misappropriated in disease. We are particularly interested in the roles of protein disorder, regulatory DNA element clustering, and non-coding RNA in nuclear condensate formation and function.
Hesham Sadek, M.D., Ph.D.
We have recently made a number of fundamental observations outlining the transient regenerative potential of the newborn mammalian heart and the role of cardiomyocyte proliferation in heart regeneration. We are currently focusing on identifying mechanisms of cardiomyocyte cell cycle regulation and developing strategies to reawaken the regenerative potential of the adult heart.
Matthew Sieber, Ph.D.
My lab uses a multisystem approach to study the metabolic basis for development and disease. Our research focuses on three main questions: 1) Defining the metabolic mechanisms that underlie cellular quiescence and reactivation. 2) Examining how dynamic changes in the mitochondrial metabolism support growth and differentiation. 3) Examining how changes in metabolism and dietary nutrients influence the regulation of conserved pathways that control development and disease progression.
Lu Sun, Ph.D.
We study the most numerous but mysterious cells in the brain, called “glial cells”. We aim to identify the fundamental principles governing glial development and neuron-glial interactions in health and disease. This will help us better characterize many neurological disorders that are greatly contributed by glial dysfunction, including white matter injury, multiple sclerosis, brain tumors, and Alzheimer’s disease.
Vincent Tagliabracci, Ph.D.
The Tagliabracci Lab uses bioinformatics, biochemistry and structural biology to study an important family of enzymes known as protein kinases. These enzymes play critical roles during tissue regeneration in response to injury or disease. Protein kinases are an important group of drug targets and understanding how these enzymes function at the molecular level can lead to treatments for tissue regeneration and other human diseases.
Nicolai van Oers, Ph.D.
We are interested in understanding the molecular mechanisms that regulate the development of the thymus under normal and disease states. One human disorder that results in a hypoplasia of the thymus is 22q11.2 deletion syndrome. We are using mouse models of this order along with thymic tissues from patients with the goal of regenerating normal thymic tissue functions. The studies will enable us to identify the molecular mechanisms required for thymus regeneration.
Yihong Wan, Ph.D.
Using genetic, molecular and pharmacological tools, we decipher new biological principles governing hematopoietic and mesenchymal stem cells, particularly the differentiation of osteoclast and osteoblast in the context of bone regeneration, osteoporosis and cancer bone metastasis.
Katherine Wert, Ph.D.
The overall research goal of the Wert laboratory is to discover and understand the genetic mechanisms underlying neuro-retinal disease, and to provide novel therapeutics for these complex degenerative disorders using gene therapy and genome engineering technologies, human stem cell transplantations, and metabolic rescue.
Thomas Wilkie, Ph.D.
The Wilkie lab is working on liver and pancreas regeneration from transplanted stem cells of the hepatopancreatic duct, metabolic stress signaling in stem cells, and early detection and therapeutics for pancreatic ductal adenocarcinoma.
Carol Wise, Ph.D.
The Wise Lab is interested in the mechanisms that regulate musculoskeletal development, remodeling, and repair. We use genomic methods to uncover the mutations that disrupt these processes and cause developmental disorders in children. We are particularly interested in identifying novel therapeutic targets to improve bone quality and regeneration.
Ann Word, M.D.
The Word Lab seeks to define the molecular, matricellular, and hormonal machinery that controls regeneration and repair of the injured vaginal wall after childbirth or surgery. We use mouse models of pelvic organ prolapse and animal models of injury to optimize matrix regeneration of the female pelvic floor.
Jun Wu, Ph.D.
Interspecies chimeras are excellent models for studying developmental biology in an evolutionary context, understanding body- and organ-size determination, probing species’ specific behavioral traits, and uncovering molecular basis of species barriers. The Wu lab is interested in applying cutting edge stem cell and genome/epi-genome editing technologies for the generation of interspecies chimeras to gain novel insights in basic biology and develop new translational applications.
Jian Xu, Ph.D.
Our research focuses on the intersection of transcriptional control with stem cell biology, hematopoiesis, and cancer. We investigate the role of non-coding cis-elements including enhancers and associated chromatin regulators in blood stem cell development. It is our long-term goal to elucidate the principles of gene regulation to facilitate the development of mechanism-based cancer therapeutics.
Chun-Li Zhang, Ph.D.
Our laboratory is interested in understanding the genetic and epigenetic regulation of neurogenesis in adult brain and spinal cord. Through modulating and inducing endogenous neurogenesis, we hope to empower the central nervous system to repair itself following post-traumatic injuries or degeneration. A second line of research uses reprogrammed human motor neurons as a therapeutic approach for human neural degenerative diseases.
Hao Zhu, M.D.
We aim to define the genetic and cellular machinery that controls regenerative capacity and injury resistance in the liver. With this knowledge, we have developed mouse models that possess enhanced mammalian regeneration in the liver and in other organs. Ultimately, we will ask how such improvements in mammalian regeneration influences cancer formation.