Rockefeller University
Appointed in 1947
University of California, Los Angeles
Appointed in 1997
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University of California, Los Angeles
Appointed in 1997
Harvard University Medical School
Appointed in 2005
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Harvard University Medical School
Appointed in 2005
Massachusetts Institute of Technology
Appointed in 1997
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Massachusetts Institute of Technology
Appointed in 1997
Northwestern University
Appointed in 2008
Carnegie Institute for Science
Appointed in 1994
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Carnegie Institute for Science
Appointed in 1994
Johns Hopkins University
Appointed in 1995
University of California, Berkeley
Appointed in 1968
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University of California, Berkeley
Appointed in 1968
University of North Carolina
Appointed in 1982
Harvard University
Appointed in 1987
La Jolla Institute for Allergy and Immunology
Appointed in 2012
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La Jolla Institute for Allergy and Immunology
Appointed in 2012
Yale University
Appointed in 2016
University of California, Berkeley
Appointed in 1957
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University of California, Berkeley
Appointed in 1957
Harvard University
Appointed in 1980
Harvard University Medical School
Appointed in 1981
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Harvard University Medical School
Appointed in 1981
University of Wisconsin, Madison
Appointed in 1965
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University of Wisconsin, Madison
Appointed in 1965
Stanford University
Appointed in 1971
University of California, San Diego
Appointed in 1972
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University of California, San Diego
Appointed in 1972
Rockefeller University
Appointed in 2011
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Rockefeller University
Appointed in 2011
Pennsylvania State University
Appointed in 2000
Massachusetts Institute of Technology
Appointed in 2001
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Massachusetts Institute of Technology
Appointed in 2001
University of California, San Francisco
Appointed in 1988
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University of California, San Francisco
Appointed in 1988
MRC Center, University Medical School, England
Appointed in 1969
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MRC Center, University Medical School, England
Appointed in 1969
University of Washington
Appointed in 2022
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University of Washington
Appointed in 2022
The innate immune system is paramount in recognizing foreign or mutated material and initiating proper immune responses to combat them. Recognition of allergens and parasitic worms (helminths) elicit a socalled “type 2” immune response focused on expulsion of stimuli and tissue repair. Type 2 immune responses impact the prognosis of many cancers and the success of immunotherapies, but how these responses are established remains poorly understood. Group 2 innate lymphoid cells (ILC2s) initiate and propagate type 2 immune responses, but do not sense immune agonists directly. The origin and regulation of host-derived signals leading to ILC2 activation is therefore an area of immense interest. Recent work identified a specialized population of epithelial tuft cells responsible for sensing helminths and activating ILC2s by secreting interleukin(IL)-25 and cysteinyl leukotrienes in the small intestine. Airway ILC2s are similarly important for type 2 immune responses in the lung, but tuft cells are dispensable in this context. My proposal seeks to identify the signals that activate intestinal tuft cells and a novel cell subset responsible for airway ILC2 activation. Examining the initiation of type 2 immunity in multiple organs will uncover both convergent and divergent mechanisms by which type 2 responses can be further manipulated.
Stanford University
Appointed in 1977
Harvard University Medical School
Appointed in 1971
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Harvard University Medical School
Appointed in 1971
University of California, Los Angeles /
University of Basel, Switzerland
Appointed in 1983
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University of California, Los Angeles / University of Basel, Switzerland
Appointed in 1983
Stanford University
Appointed in 1985
California Institute of Technology /
Yale University
Appointed in 1976
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California Institute of Technology / Yale University
Appointed in 1976
University of California, San Diego
Appointed in 1981
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University of California, San Diego
Appointed in 1981
Weizmann Institute of Science, Israel
Appointed in 1968
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Weizmann Institute of Science, Israel
Appointed in 1968
University of California, Berkeley
Appointed in 2005
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University of California, Berkeley
Appointed in 2005
University of Copenhagen, Denmark /
Cambridge University, England
Appointed in 1949
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University of Copenhagen, Denmark / Cambridge University, England
Appointed in 1949
Harvard University
Appointed in 2011
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Harvard University
Appointed in 2011
Stanford University
Appointed in 2000
Harvard University Medical School
Appointed in 1992
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Harvard University Medical School
Appointed in 1992
Massachusetts General Hospital
Appointed in 2017
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Massachusetts General Hospital
Appointed in 2017
Molecular oxygen presents a fundamental biological problem: it is vital for life, yet also incredibly toxic. As the terminal electron acceptor in aerobic respiration and the redox engine of mitochondria, oxygen provides eukaryotes with the vast majority of their energy. However when molecular oxygen is reduced it can form damaging reactive species, and recent work has demonstrated that animals with genetic lesions in the mitochondrial respiratory chain are extremely vulnerable to oxygen toxicity. How animals have evolved to manage this double-edged sword remains a fundamental question._x000D_
The biology and natural ecology of the nematode C. elegans make it an attractive system in which to study oxygen tolerance. Wild type C. elegans are tolerant of oxygen concentrations ranging from 1% to 100%, and years of genetic studies have generated a rich toolbox of mitochondrial mutants. I will use these mutants to study the biology of oxygen tolerance, which may simultaneously shed light on the connection between mitochondrial disease and oxygen toxicity.
Massachusetts General Hospital
Appointed in 2005
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Massachusetts General Hospital
Appointed in 2005
Brigham and Women's Hospital
Appointed in 2020
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Brigham and Women's Hospital
Appointed in 2020
Ubiquitylation is a post-translational modification that regulates the stability of thousands of proteins in our cells. The specificity for ubiquitylation is typically conferred by E3 ubiquitin ligases that attach ubiquitin onto substrate proteins. Despite the critical role that ubiquitylation plays in regulating the abundance and activity of many proteins, most ubiquitylation pathways are still poorly understood and many of the estimated ~600 E3 ubiquitin ligases have no known protein substrates.
Our lab has developed the Global Protein Stability (GPS) assay, which is a way to rapidly monitor protein stability using fluorescent proteins. We have recently been adapting this approach for library-on-library genetic screens in order to map, in parallel, dozens of ubiquitylation substrates to their cognate E3 ubiquitin ligases. We have also been using GPS screens to find degradation pathways specific to particular intracellular compartments. Together, these approaches will shed light on ubiquitylation pathways that are important for human health.
University of Cambridge, England
Appointed in 1957
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University of Cambridge, England
Appointed in 1957
University of California, Santa Barbara /
Scripps Research Institute
Appointed in 1985
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University of California, Santa Barbara / Scripps Research Institute
Appointed in 1985
Dana-Farber Cancer Institute
Appointed in 2021
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Dana-Farber Cancer Institute
Appointed in 2021
Long interspersed element-1 (LINE-1) is the only active, protein-coding transposon in humans. LINE-1 overexpression and LINE-1 retrotransposition are hallmarks of human cancers, although the impact of LINE-1 activity on cancer genomes and cancer cell growth remains poorly understood. My research focuses on addressing the hypothesis that LINE-1 retrotransposition causes substantial gross genome instability in cancers. Supporting this hypothesis, a recent pan-cancer analysis demonstrated associations between somatically-acquired LINE-1 insertions and segmental copy-number changes. Moreover, our lab recently identified that the Fanconi anemia/ BRCA pathway is required for growth of LINE-1(+) cells, suggesting that this DNA repair pathway might limit genotoxic effects of LINE-1. I am developing several approaches to assess the impact of LINE-1 on genome integrity, and I am evaluating the contribution of the FA/ BRCA pathway to LINE-1-associated DNA damage. These studies will be the first to evaluate the scope of LINE-1-mediated genome instability and should inform efforts to exploit LINE-1 genotoxicity as a cancer therapeutic strategy.
Harvard University Medical School
Appointed in 2008
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Harvard University Medical School
Appointed in 2008
The sleep disorder narcolepsy is caused by the degeneration of hypocretin neurons. The goal of my research is to derive hypocretin neurons from narcoleptic patients to study the cause of hypocretin neuron loss.
I was born in Konstanz, Germany and moved to Minnesota at an early age. As a teenager, I decided I wanted to become a neurosurgeon and spent my summers in a neurosurgery laboratory. I discovered I preferred working at the bench and, as an undergraduate at Caltech, I explored different fields of neuroscience. I was most fascinated by the problem of how the brain develops, and studied the lineage and organization of neural stem cells and their progeny in the postnatal brain. My current work combines my interests in cell type specification, the connection of circuitry to behavior, and developing in-vitro models of human diseases. In my free time, I enjoy hiking, cycling, cooking, and bartending.
Institut Pasteur, France
Appointed in 1973
Stanford University /
MRC Center, University Medical School, UK
Appointed in 1973
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Stanford University / MRC Center, University Medical School, UK
Appointed in 1973
New York University
Appointed in 2017
Several vertebrate species have the astonishing ability to regenerate their limbs following amputation. In mammals, including both mice and humans, this regenerative capability has been restricted to the digit tip. Both digit tip and complete limb regeneration follow a stereotypic process termed epimorphic regeneration where a population of progenitor cells, termed the blastema, form at the injury site to replace the multiple tissues lost (including blood vessels, nerves, bone, etc.). Several studies have demonstrated that macrophages are essential for epimorphic regeneration. However, it remains largely unknown how macrophages facilitate blastema rather than scar formation. Utilizing the mouse digit tip, which displays regenerative or scarring outcomes dependent on amputation site, we are functionally testing which immune cell types uniquely contribute to epimorphic regeneration. Furthermore, by combining diverse genetic tools with intravital imaging, we are beginning to understand how injury-induced inflammation yields a permissive tissue environment for epimorphic regeneration in mammals.
University of California, San Francisco
Appointed in 2009
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University of California, San Francisco
Appointed in 2009
Harvard University Medical School
Appointed in 2017
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Harvard University Medical School
Appointed in 2017
DNA interstrand cross-links (ICLs) covalently connect the two strands of DNA, thereby blocking essential processes including DNA replication and transcription. Cells have evolved intricate pathways to repair ICLs and other DNA lesions to ensure genome integrity. In the Walter laboratory, we use egg extracts from the African clawed frog Xenopus laevis to biochemically dissect the molecular events during DNA replication and repair. Importantly, these and other processes are faithfully recapitulated in this highly tractable cell-free system._x000D_
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My current work focuses on how different lesions, including ICLs, are repaired in a transcription-dependent manner. Although Xenopus egg extracts are generally considered to be transcriptionally quiescent, I set out to develop an in vitro transcription system to eventually investigate transcription-coupled DNA repair pathways of chemically distinct lesions. My study aims to biochemically characterize the underlying mechanisms as well as to identify novel factors involved in transcription-coupled DNA repair._x000D_
Stanford University
Appointed in 1977
Rockefeller University
Appointed in 2016
My research interest is to harness the power of immune system to combat cancer. This goal requires sophisticated understanding in both immunology and cancer biology. My prior graduate training has equipped me with extensive knowledge in immunology, and showed me how the immune system evokes robust and multilayered responses to defend our body against infections. However, compared to the vigorous response to infections, the immune system often becomes incompetent when it encounters cancer, especially malignant tumors. My goal during the fellowship period is to develop a cancer model in which I can trace the co-evolution between tumor-initiating stem cells and immune system, ultimately to the point of evasion of immune surveillance, so that I can identify the root of the blunted ant-tumor immune response during the cancer progression. With Dr. Fuchs’ expertise in epithelial stem cells and cancers, and my background in immunology, I feel that I’m uniquely poised to tackle this fascinating problem.
University of California, San Francisco
Appointed in 1983
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University of California, San Francisco
Appointed in 1983