Boston Children's Hospital
Appointed in 2020
Advancements in vaccine design and immunotherapy have helped us gain insights into how to promote immunity against infections or cancers. However, excessive inflammation associated with immunotherapies, autoimmune diseases, non-healing wounds and even COVID19 is currently at the center of healthcare challenges. Following an inflammatory insult, such as an injury or pathogen invasion, immune cells in the tissues are crucial to resolve inflammation and regain healthy tissue function. Damaging inflammatory signals also activate nearby high threshold sensory neurons– the nociceptors – which are responsible for initiating pain and guarding/withdrawal responses which is believed to prevent further tissue damage. While it is conceivable that nociceptors can cooperate with immune to promote healing, the role of these neurons in shaping the healthy immune landscape of barrier tissues is currently unexplored. In the Woolf lab, I aim to determine the role of nociceptor sensory neurons in restoring the healthy immune profile of barrier tissues following an adverse and painful inflammatory event and develop novel strategies to manipulate neuroimmune interactions using genetic and pharmacological methods. Traditionally, inflammatory conditions are treated with broad immunosuppressants that put the patients at risk for further infections. The ability to fine tune immune function by controlling specific neuronal signals will offer a safer and effective therapeutic strategy for various inflammatory diseases as well as malignancies.
University of California, Los Angeles
Appointed in 2016
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University of California, Los Angeles
Appointed in 2016
The mitochondrion is a subcellular organelle that is the center of energy production, calcium signaling, apoptosis and redox balance for the cell. Therefore, many diseases and normal aging run their molecular course through the mitochondrion. Uniquely, the mitochondrion contains its own DNA and makes RNA and proteins independently from the rest of the cell. This orthogonal system had presented a problem for studying the mitochondrion as the usual genetic tools of the nuclear genome are not available. However, I am using the tools of synthetic biology to allow specific interrogation of mitochondrial protein synthesis in healthy and diseased human cells._x000D_
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In addition to studying mitochondrial protein synthesis, I am developing the yeast mitochondrion as a platform for synthetic biology in order to greatly expand the genetic code and to speed up laboratory evolution. These tools will allow creation of novel therapeutic biopolymers and proteins.
University of California, San Francisco
Appointed in 1983
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University of California, San Francisco
Appointed in 1983
Stanford University
Appointed in 1984
University of Wisconsin, Madison
Appointed in 1990
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University of Wisconsin, Madison
Appointed in 1990
University of California, San Francisco
Appointed in 2008
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University of California, San Francisco
Appointed in 2008
My research involves the reconstruction of the T-cell antigen receptor signaling pathway in an orthogonal cell line to piece apart the molecular details of immune cell triggering, and how the system’s specificity and sensitivity can be genetically encoded.
I am originally from England and did both my undergraduate biochemistry degree and doctoral work at the University of Oxford. Throughout this period, my thoughts became increasingly focused on how signals are transmitted across the impermeable cell membrane, especially where the receptor responsible has no enzymatic activity of its own. For me, this area of research combines cell biology, biochemistry and systems analysis into one very exciting topic which, when applied to cells of the immune system, can have clear implications for new points of therapeutic intervention. Relocating to San Francisco for my postdoc has also provided me with great insights into the similarities and differences between approaches to scientific research on opposite sides of the Atlantic. I hope to combine the best of both worlds when starting my independent career in the near future.
Yale University
Appointed in 1979
Stanford University
Appointed in 2010
Working in the lab of K. Christopher Garcia, I am studying the assembly and three-dimensional structures of Wnt-receptor complexes in order to understand Wnt signaling mechanisms, and facilitate development of new strategies to clinically target Wnt-associated diseases.
I have always enjoyed studying biological problems, particularly using structural and biochemical methods to understand underlying molecular mechanisms.  I am most fascinated by fundamental and hard problems that require creativity, tenacity and dedication to solve.  After having studied fundamental aspects of protein translocation, I now wish to examine receptor-ligand interactions with high relevance to human disease. Wnt signaling is important in many developmental and regenerative processes, and in a variety of human diseases, including many types of cancers. However, due to major technical difficulties, there is a complete lack of extracellular structural information about Wnt signaling activation and inhibition. We are using traditional and novel methodologies to obtain structural information that can ultimately facilitate the development of new strategies to therapeutically target Wnt signaling. Most of my spare time is spent running over the hills behind Stanford to train for a marathon, relax from hard work, and think about new ways to approach scientific problems.
Stanford University
Appointed in 1985
University of California, Berkeley
Appointed in 1968
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University of California, Berkeley
Appointed in 1968
Montefiore Hospital
Appointed in 1961
Columbia University
Appointed in 1971
Cold Spring Harbor Laboratory
Appointed in 1971
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Cold Spring Harbor Laboratory
Appointed in 1971
Columbia University
Appointed in 2017
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Columbia University
Appointed in 2017
The genetic diversity within microbial populations provides important means for the organisms to survive in fluctuating environments. Studying such diversity helps to elucidate how mutations within population interact with each other, and how the host microbes harboring them adapt and evolve to extreme environments such the presence of antibiotics. Although whole genome sequencing can readily detect all mutations at a population level, methods that can quantify the abundance of mutations at both the population and single-cell resolution are lacking. Here I propose to implement a CRISPR-Cas system that works as both a transcriptional perturbation and a molecular recording device in bacteria. This technology can rapidly and continuously generate highly diverse knock-down variants among a microbial population_x000D_
while it is adapting to extreme environments that pose significant fitness challenges. Combined with deep sequencing of the CRISPR “memory cassette”, the transcriptional perturbation and the evolutionary trajectories in each individual cells of the population can be quantified and followed, respectively. Results_x000D_
obtained from this method can also shed light on epistatic interactions and contingencies between mutations, and reveal novel regulatory pathways that are important for antibiotic resistance.
Massachusetts Institute of Technology
Appointed in 1991
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Massachusetts Institute of Technology
Appointed in 1991
Rockefeller University
Appointed in 1971
Albert Einstein College of Medicine
Appointed in 1972
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Albert Einstein College of Medicine
Appointed in 1972
University of California, San Francisco
Appointed in 1993
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University of California, San Francisco
Appointed in 1993
California Institute of Technology
Appointed in 1996
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California Institute of Technology
Appointed in 1996
University of California, San Francisco
Appointed in 2014
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University of California, San Francisco
Appointed in 2014
Rockefeller University
Appointed in 2016
Resistance to chemotherapeutic drugs is a major obstacle in the successful treatment of many different forms of cancer. This so-called multidrug resistance is often mediated by a class of proteins known as ABC transporters. These proteins reside in the plasma membrane and actively pump molecules out of the cell by utilizing the energy of ATP binding and hydrolysis. Some ABC transporters recognize and extrude anticancer compounds before they are able to kill the cancer cells, leading to drug resistance and treatment failure._x000D_
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My project seeks to gain a better mechanistic understanding of these transporters and their role in multidrug resistance by utilizing a combination of structural and functional studies. My focus will be on the ABC transporter known as multidrug resistance protein 1 (MRP1). If we can better understand how these proteins are able to recognize and transport their drug substrates, we will be able to develop ways to block or circumvent their function during cancer treatment. If successful, these studies will not only further our knowledge of ABC transporter biology, but they will also lay a framework for combating multidrug resistance in cancer patients.
New York University
Appointed in 2006
University of California, Berkeley
Appointed in 1976
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University of California, Berkeley
Appointed in 1976
Harvard University Medical School
Appointed in 2005
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Harvard University Medical School
Appointed in 2005
California Institute of Technology
Appointed in 1992
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California Institute of Technology
Appointed in 1992
New York University
Appointed in 2000
Harvard University
Appointed in 2019
Infant vocalization is a pervasive mammalian social behavior that elicits parental care essential for infant health. Features of infant vocalization are innate, heritable, and vary between species, but we know little about the genetic or neural mechanisms underlying this variation. To better understand these mechanisms, I study the cries of infant Peromyscus mice (also known as deer mice), a group of closely related rodents that have recently diversified across North America and evolved a range of heritable behaviors. Deer mice are attractive systems to understand natural variation in infant vocal behaviors because interfertile species exhibit infant cries that differ in their spectral and temporal features, opening the possibility to map the genetic basis of natural variation in these features. Using approaches from neuroscience, genetics, and ethology, my work aims to make explicit mechanistic links between genes, neurons and a conserved mammalian behavior essential for early life health in rodents and humans alike.
Columbia University
Appointed in 1984
Yale University
Appointed in 1987
National Jewish Center for Immunology and Respiratory Medicine
Appointed in 1994
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National Jewish Center for Immunology and Respiratory Medicine
Appointed in 1994
Harvard University
Appointed in 1966
Stanford University /
Rockefeller University
Appointed in 2010
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Stanford University / Rockefeller University
Appointed in 2010
Stanford University
Appointed in 2018
Imperial Cancer Research Fund Laboratories, England
Appointed in 1974
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Imperial Cancer Research Fund Laboratories, England
Appointed in 1974
University of California, San Francisco
Appointed in 2010
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University of California, San Francisco
Appointed in 2010
Yale University
Appointed in 1996
University of California, Berkeley
Appointed in 1990
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University of California, Berkeley
Appointed in 1990
Brigham and Women's Hospital /
Harvard University Medical School
Appointed in 2011
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Brigham and Women's Hospital / Harvard University Medical School
Appointed in 2011
La Jolla Institute for Allergy and Immunology
Appointed in 2012
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La Jolla Institute for Allergy and Immunology
Appointed in 2012
Harvard University
Appointed in 2023
Many animals are capable of whole-body regeneration, enabling the regrowth of missing structures to their original size and shape after major amputation. Most studies investigating this phenomenon have focused on the transcriptional control of differentiation from adult pluripotent stem cells. However, Dr. Allison Kann predicts that an important, yet underappreciated, aspect of regeneration is the role of cell adhesion. Regeneration from stem cells requires free progenitor cells to unite and integrate into multicellular tissues and organs. Dr. Kann will use Hofstenia miamia, a genetically tractable invertebrate model system to investigate the disassembly, formation, and remodeling of cellular junctions during regeneration. Kann will conduct these studies in Dr. Mansi Srivastava’s lab at Harvard University. These studies will reveal new principles of regeneration and identify mechanisms that cells use to converge into multicellular structures.
As a graduate student in Dr. Robert Krauss’ lab at Icahn School of Medicine at Mount Sinai, Kann investigated the activation of muscle stem cells. She identified that cytoskeletal regulation is a key driver of muscle stem cell fate decisions and demonstrated how stem cells transduce injury signals into activation. With her background in adult stem cell biology, Dr. Kann is now ready to investigate how cellular interactions between progenitor cells regulate organismal regeneration.
Stanford University
Appointed in 1986
Massachusetts Institute of Technology
Appointed in 1989
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Massachusetts Institute of Technology
Appointed in 1989
Harvard University
Appointed in 2020
Mammalian social behaviors change dramatically over the lifespan: infants rely on their mothers for food and warmth, adolescents engage each other in social play, and adults mate and parent. This highly conserved social niche trajectory consists of dynamic motivational drives and behavioral repertoires and co-occurs alongside rapid changes in brain organization. However, it remains unclear how developmental changes in behavior result from transformations of the underlying brain circuits.
As a postdoctoral fellow in Catherine Dulac’s lab, I am dissecting these developmental transitions in mammalian brain and behavior. Focusing on the mouse hypothalamus, I am charting the coordinated emergence of transcriptional cell-type identities, spontaneous and stimulus-evoked neuronal activity patterns, and corresponding changes in behavior. Further, I am exploring the robustness and plasticity of these trajectories by manipulating the animal’s sensory and social rearing environment. This work will provide novel insights into the developmental processes that build animal behavior.
MD Anderson Cancer Center
Appointed in 2013
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MD Anderson Cancer Center
Appointed in 2013
University of California, San Diego
Appointed in 2020
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University of California, San Diego
Appointed in 2020
Memorial Hospital, New York
Appointed in 1946
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Memorial Hospital, New York
Appointed in 1946
University of Cambridge, England
Appointed in 1978
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University of Cambridge, England
Appointed in 1978
University of California, San Francisco
Appointed in 1981
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University of California, San Francisco
Appointed in 1981
Indiana University
Appointed in 1976
Stanford University
Appointed in 2018
A lesson of the genome wide association study (GWAS) era is that _x000D_
approximately 90% of causal disease variants influence gene expression. Mapping genetic variants that influence molecular-level phenotypes has elucidated various mechanisms underlying gene expression diversity. Recently, we showed that genetic variants coordinate histone modifications at sites of intra-chromosomal interaction, thereby providing a mechanism for variation in the activity of regulatory elements that lack local sequence variation [15]. We hypothesize that genetic variants influence distal sites by affecting the stability of chromosomal contacts (“loops”) and that this is a common mechanism for gene expression variation. The_x000D_
location of loops is sequence-specific, mediated by transcription factors (TFs) that bind specific DNA motifs. Genetic variants that disrupt binding sites could therefore be expected to destabilize loops and prevent enhancer-promoter contacts. We propose to map genetic variants affecting chromosomal interactions in order to characterize this novel mechanism for gene expression diversity. We will employ an efficient pooling strategy, which will enable us to map variants in an expanded set of 1000 people belonging to 10 populations. We will leverage the genetic loci we identify to fine-map GWAS hits and discover causal variants that confer disease risk through effects on 3D genome architecture.
University of California, San Francisco
Appointed in 2016
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University of California, San Francisco
Appointed in 2016
Memory informs how animals interact with the world. It provides an expectation of the future based upon past experience. With navigation, animals draw upon a memory of their surroundings to inform their decisions. The hippocampus is critical for spatial decision-making by providing multiple ways to recall surroundings. Yet, why the hippocampus has multiple recall strategies remains unknown. To test the hypothesis that different recall strategies provide the substrate for individual variability, I will explore the behavior and hippocampal neural activity of both male and female rats during different spatial tasks. Beyond just recording the differences between animals, I will also specifically block hippocampal recall activity to determine their necessity for individual behavior. Studying individual decision-making will explore the range of neural computations that are consistent with normal functioning, and further our understanding of the complex relationship between the internal representation of the world and its external manifestations