Rockefeller University
Appointed in 2016
Dissecting the immune evasion mechanisms of tumorigenic stem cells
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
Modulation of gene expression by regulatory proteins
Scripps Research Institute
Appointed in 2006
Kinetic analysis of 30S ribosomal subunit assembly
Massachusetts Institute of Technology
Appointed in 1990
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Massachusetts Institute of Technology
Appointed in 1990
Protein folding information in the Arc repressor
Harvard University Medical School
Appointed in 1998
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Harvard University Medical School
Appointed in 1998
Chemical inhibition of microtubule nucleation
University of California, Berkeley
Appointed in 2000
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University of California, Berkeley
Appointed in 2000
In vitro reconstitution of golgi biogenesis in S. cerivisiae
Stanford University School of Medicine
Appointed in 2002
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Stanford University School of Medicine
Appointed in 2002
Developmental genetics of stickleback raker number
Harvard University
Appointed in 1986
Biochemistry of cell type control in yeast
The Ragon Institute of MGH, MIT, and Harvard
Appointed in 2025
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The Ragon Institute of MGH, MIT, and Harvard
Appointed in 2025
A spatial stochasticity theory resolves how host-protective T cell responses emerge amid regulatory T cell immunosuppression
Dr. Tomer Milo appreciates distilling simplicity out of complex biological systems. During his graduate work, Milo developed elegant theories for a variety of human diseases and collaborated with experimentalists to validate them. In his fellowship he will develop his own experimental expertise and combine it with his theoretical expertise to tease apart immune processing of self vs. foreign antigens.
During Dr. Milo’s thesis research in Dr. Uri Alon’s lab at the Weizmann Institute of Science he “studied design principles of physiological systems to better understand complex human diseases.” His work provided groundbreaking insight into the tumor microenvironment, bipolar disorder, and autoimmune disease. In his work, Milo used mathematical modeling to identify molecular players and cellular interactions critical in a host of biological diseases.
As a postdoc in Dr. Harikesh Wong’s lab at the Ragon Institute and Mass General, Dr. Milo will focus on systems immunology. Milo will investigate how a specific immune cell population, regulatory T cells, prevents autoimmune responses to self antigens while allowing appropriate immune responses against pathogenic non-self antigens. He thinks that the spatial segregation of the lymph node is crucial for this discrimination and will use high-resolution imaging and mouse models to tackle this question. Milo’s research will answer critical and fundamental questions in immune biology and provide insight into immune responses at homeostasis, during infection, and in autoimmune disorders.
Cold Spring Harbor Laboratory
Appointed in 1993
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Cold Spring Harbor Laboratory
Appointed in 1993
Regulation of eukaryotic DNA replication
Rockefeller University
Appointed in 1967
Mechanism of suppression or rg mutant in Neurospora
California Institute of Technology
Appointed in 2010
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California Institute of Technology
Appointed in 2010
Regulation of mitochondrial fusion
I am investigating mechanisms of mitochondrial fusion within cells. The goal is to gain a better understanding of how mitochondrial dynamics are regulated.
My interest in scientific research began when I was young, and was fostered through participation in research programs and science fairs in junior high and high school. ¬†After completing my bachelor’s degree in biochemical sciences at Harvard University, I worked briefly for a biotechnology company developing treatments for patients suffering from rare genetic disorders. ¬†I then entered an MD/PhD program the University of Texas Southwestern Medical Center, allowing me to conduct basic science research while receiving training in patient care. ¬†I currently conduct research as a postdoctoral fellow at the California Institute of Technology, and plan to establish my own basic science laboratory in the future.
University of California, San Francisco
Appointed in 1998
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University of California, San Francisco
Appointed in 1998
A screen for axon guidance molecules in mouse
University of California, Berkeley
Appointed in 2016
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University of California, Berkeley
Appointed in 2016
Pathogen-driven evolution of inflammasome genes
Yale University
Appointed in 1981
DNA topology in viruses
Yale University
Appointed in 2004
University of California, San Diego
Appointed in 2015
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University of California, San Diego
Appointed in 2015
Top-down modulation of visual cortex during attention
Yale University
Appointed in 1963
Structure and hormonal responses of mammary glands of embryonic components
Rockefeller University
Appointed in 2014
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Rockefeller University
Appointed in 2014
Self vs. non-self discrimination during CRISPR-Cas adaptive immunity
University of California, Berkeley
Appointed in 2015
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University of California, Berkeley
Appointed in 2015
Intra and trans-cellular mitochondrial communication in Parkinson's disease
Just like people, cells have to deal with stress. I study how stressed cellular organelles such as mitochondria communicate with the nucleus, and how this stress response is coordinated in normal settings and dysregulated in disease._x000D_
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I studied genetics as an undergraduate at the University of California, Berkeley, and then worked at Sangamo BioSciences to help develop human genome editing with engineered nucleases. I was then an NSF Fellow in the Tetrad PhD program at the University of California, San Francisco, where I worked in Christine Guthries laboratory. There, I studied how pre-mRNA splicing is regulated in particular, how the cell coordinates a pre-mRNAs transcription and its splicing. My interest in how discrete molecular processes are integrated inside the cell continues during my postdoctoral fellowship in Andrew Dillins laboratory, where I am studying a remarkable pathway called the mitochondrial unfolded protein response. In this pathway, nuclear-encoded mitochondrial protein chaperones are upregulated in response to signals from mitochondria experiencing proteotoxic stress. I am using a disease-in-a-dish model that combines human stem cell technology with genome editing approaches.
Rockefeller University
Appointed in 2011
Defining layers of post-transcriptional control in chronic inflammatory disease
Harvard University
Appointed in 2015
Neuronal control of suckling behavior in newborn rodents
My research investigates the neural circuits that control instinctive behavior. Previously, my work focused on the innate active sensing behaviors of rodents that dominate exploration and social interactions. This work has led me to focus on questions that involve the nature of the motivational and descending drives that enable animals to generate robust and instinctive motor patterns in the appropriate context. With the expertise of the Dulac Laboratory, I hope to provide insight into these questions by defining the roles of specific, molecularly-defined cell types and neuronal circuit connectivity patterns that relate to such control. I hope to provide a unique perspective that stems from a background in engineering and the neural control of movement.
University of Oregon
Appointed in 1988
In vitro assay for Golgi to vacuole transport utilizing all yeast components
University of Utah
Appointed in 2019
The eukaryotic RNA-metabolite interactome and its role in gene regulation
The ability of cells and organisms to sense and respond to change is fundamentally driven by dynamic interactions between many different types of molecules. Although we understand some of these interactions, there are many to be uncovered.
I am investigating the landscape of RNA-metabolite interactions and their role in gene regulation. Although RNAs and small molecules can form specific and high-affinity interactions, we know effectively nothing of the RNA-metabolite interactome that might be present in eukaryotic cells. Using RNA-structure probing technologies coupled with high-throughput sequencing, I am studying a broad pool of human RNAs in various metabolic contexts, which will uncover the scope of interactions between human RNAs and human metabolites, identify the specific RNA-metabolite interactions that do occur, and allow us to test the role of these interactions in gene regulation. In complement to this approach, we have developed a screening platform to simultaneously measure the affinity between specific RNAs and 450+ human metabolites. This platform has allowed for rapid, targeted screening of viral RNAs that might sense host metabolism via RNA-metabolite interactions and can be applied to any RNA of interest.
Yale University
Appointed in 1988
Primer recognition properties of the human telomere terminal transferase enzyme
University of Connecticut Health Center
Appointed in 1975
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University of Connecticut Health Center
Appointed in 1975
Surfaces of cells of nervous tissues
University of California, San Francisco
Appointed in 2019
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University of California, San Francisco
Appointed in 2019
Structural studies of membrane fission and highly constricted membranes
Harvard University Medical School
Appointed in 1998
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Harvard University Medical School
Appointed in 1998
Molecular mechanism of retroviral fusion
University of California, Berkeley
Appointed in 1983
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University of California, Berkeley
Appointed in 1983
X-ray crystallographic studies of chemotaxis receptors
University of California, Davis
Appointed in 1958
Biosynthesis of unsaturated fatty acids
Harvard University
Appointed in 2015
Live cell imaging of chromatin supercoiling dynamics in human cells
I received my BS in Biochemistry from Susquehanna University and my Ph.D. in molecular biophysics in Professor Scott Baileys lab at Johns Hopkins University. Broadly speaking, I am interested in exploring the structure-function relationship of biological macromolecules. For my Ph.D. thesis, I used different structural and biochemical methods to investigate the mechanism by which bacteria use their CRISPR immune system to destroy foreign DNA._x000D_
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In my postdoc with Professor Sunney Xie at Harvard University, my research focuses on the effects of chromatin structure on eukaryotic gene expression. More specifically, I am interested in understanding the dynamics of DNA supercoiling at a single-cell level. Outside the lab, I enjoy playing soccer and going on hikes.
Johns Hopkins University /
The Salk Institute for Biological Studies
Appointed in 1995
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Johns Hopkins University / The Salk Institute for Biological Studies
Appointed in 1995
Biochemistry of a cortical proilin binding complex
University of Dundee, Scotland
Appointed in 1987
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University of Dundee, Scotland
Appointed in 1987
Mechanisms of Golgi-fragmentation during mitosis
Princeton University
Appointed in 1994
p53 negatively regulates a microtubule-associated protein
Yale University
Appointed in 1944
Heterologous transplantation of human tumors
University of Washington
Appointed in 2004
Embryonic single-cell gene expression in C. elegans
Harvard University
Appointed in 1981
Notch, a regulator of neural determination in D. Melanogaster
Johns Hopkins University
Appointed in 1998
Tubulogenesis during Sriosophila embryonic development
University of Wisconsin, Madison
Appointed in 1988
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University of Wisconsin, Madison
Appointed in 1988
Isolation of the tol+ gene from Neurospora crassa
University of Utah
Appointed in 2024
Ron Tyrosine Kinase deficiency uncovers a critical regulator of anti-tumor T Cell responses
Metastasis, which includes the dissemination of tumor cells from a primary site and subsequent colonization of faraway sites, is the primary cause of cancer deaths. This process requires a failure of our immune system to recognize and destroy metastasizing cancer cells. As such, targeting cancer during the metastasis step will help create therapies for patients with many different types of cancers (breast, prostate, colon, etc.).
Dr. Marija Nadjsombati will investigate the immune response during metastasis in Dr. Alana Welm’s lab at the University of Utah. Dr. Nadjsombati will use mouse models of breast cancer which faithfully recapitulate metastatic propensity. Nadjsombati will develop new cancer models and investigate their transcriptional regulatory networks to decipher the role of T cell regulation in metastasis. These studies will provide novel insights on both T cell regulation and on targeted therapies for cancer immunology.
Nadjsombati built her expertise in immunology as a graduate student in Dr. Jakob von Moltke’s lab at the University of Washington. There she studied a specialized type of epithelial cells, called tuft cells, which initiate immune responses in the small intestine. Nadjsombati discovered that succinate triggers the downstream signaling in tuft cells that initiates a type 2 immune response. Additionally, by comparing different mice strains, and performing genetic crosses, Nadjsombati showed that Pou2af2 isoform expression is a key regulatory mechanism that determines tuft cell frequency. With this strong immunological background, Nadjsombati is poised to make new breakthrough discoveries on the immune regulation of metastasis.
Yale University
Appointed in 1965
Nature of the reticulum cell and anaplastic types
Stanford University /
Massachusetts General Hospital
Appointed in 1968
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Stanford University / Massachusetts General Hospital
Appointed in 1968
Enzymatic basis of recombination
Rockefeller University
Appointed in 2025
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Rockefeller University
Appointed in 2025
A genetic approach to study metabolite sensing and regulation in organelles
Dr. Toshitaka Nakamura is interested in understanding protein-chemical interactions that mediate how cells sense stress. During his graduate work he found and characterized new compounds that kill cancer cells by triggering a type of cell death called ferroptosis. In his fellowship, he is interested in understanding how cells handle iron and glutathione, a crucial antioxidant and detoxifying agent, to mitigate stress responses.
In Dr. Nakamura’s graduate research in Dr. Marcus Conrad’s lab at Helmholtz Munich, he investigated the role of the protein ferroptosis suppressor protein (FSP1) in halting ferroptosis, a form of cell death that functions by damaging cell membranes. Nakamura discovered molecules that block FSP1, which induces cancer cell death. He showed that these molecules work by moving FSP1 away from cell membranes, inactivating the inherent enzymatic activity that protects them from damage. Then, by studying FSP1 mutations from cancer patients and lab experiments, he found another inhibitor and identified out how both types work. Collectively, his research provided groundbreaking insight into the role of FSP1 in ferroptosis, and revealed how this protein can be therapeutically targeted in cancer treatments.
Now, as a fellow in Dr. Kıvanç Birsoy’s lab at Rockefeller, Nakamura will study how cells sense metabolites in different cellular compartments. To facilitate his studies Nakamura will develop a CRISPR-Cas9-based genetic screening platform that can target specific organelles. Then, he’ll leverage his platform to investigate iron and glutathione sensing in mitochondria. In addition to providing a novel, widely applicable research tool, Nakamura’s studies may provide new insights and identify tractable therapeutic targets in diseases like cancer and neurodegeneration.
University of Rochester Medical Center
Appointed in 2026
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University of Rochester Medical Center
Appointed in 2026
In vivo mapping of lung microenvironmental interactions controlling CD8⁺ tissue-resident memory persistence
Dr. Sandra Nakandakari-Higa wants to understand how a cell’s fate and function are determined. This process is not shaped in isolation; rather, it is shaped through continuous interactions with neighboring cells, forming dynamic networks of communication that orchestrate development, homeostasis, and immune responses. As a Jane Coffin Childs Fellow, she’ll use Labeling Immune Partnerships by SorTagging Intercellular Contacts (LIPSTIC), an approach she improved in her graduate work, to evaluate the persistence of memory T cells within the lung.
Using LIPSTIC, Nakandakari-Higa studied how brief interactions between immune cells and their cellular partners shape lasting immune responses during her graduate work in Gabriel Victora’s lab at The Rockefeller University. Nakandakari-Higa redesigned LIPSTIC so it no longer depends on one specific receptor–ligand pair. This made it broadly applicable for many types of cell interactions. She used this “universal” LIPSTIC to follow how dendritic cells activate T cells and how virus-specific T cell interactions change over time, and the tool can now help other researchers track immune contacts in detail.
As a JCC Fellow in Minsoo Kim’s lab at the University of Rochester, Nakandakari-Higa will focus on a key aspect of protective immunity: the generation and persistence of memory T cells in the lung. Infection with respiratory viruses generates these T cells and provides protection against reinfection. However, over time the numbers of these T cells wane which limits their effectiveness. Nakandakari-Higa will use her universal LIPSTIC technology to map the cellular interactions of memory T cells in the lung, and to analyze how those interactions change. She’ll also invert LIPSTIC to determine how signals delivered by the local microenvironment contribute to T cell survival. Her research may provide new clues that could inform ways to make vaccine protection last longer.
Albert Einstein College of Medicine
Appointed in 1966
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Albert Einstein College of Medicine
Appointed in 1966
RNA synthesis
University of Washington
Appointed in 1978
Control of transciption in yeast
NIH/NICHD
Appointed in 2024
Awarded Sponsor: Dr. Amy Shyer
Linking Parts to Process: Probing the Cell-Biological Basis for Tissue Patterning in Developing Mesenchyme
Organismal development is an elegant progression from a single cell to billions or trillions of different cells that form our tissues and organs. While much is known about development at the molecular level, important questions remain about how subcellular molecular inputs integrate with “supracellular” physical behaviors of large cell collectives to shape our tissues. Little is known about how subcellular and supracellular dynamics relate among the mesenchymal cell types that give rise to all connective tissues including skin.
Dr. Victor Naturale will make inroads into these questions using a novel vertebrate skin cell platform developed in Dr. Amy Shyer’s and Dr. Alan Rodrigues’ lab at The Rockefeller University. Dr. Naturale expects that understanding how biological organization translates across length scales will provide novel insight into diverse areas including cancer microenvironments and mesenchymal birth defects that lack a single genetic cause.
Naturale developed his interest in developmental biology as a graduate student in Dr. Jessica Feldman’s lab at Stanford University. Working largely at the molecular to cellular scale, Naturale discovered that in C. elegans the polarity scaffold PAR-3 and the transmembrane protein HMR-1/E-cadherin collaboratively build polarity networks at epithelial cell-cell contacts. He demonstrated that HMR-1 also communicates cell polarity at the tissue level. Importantly, Naturale additionally identified a novel symmetry breaking cue arising at the supracellular scale due to emergent cell-cell contact patterns. This research, and the beautiful images within, were highlighted on the journal cover. In his postdoctoral research, Naturale will translate his experience identifying supracellular cues to a novel model system with relevance to cancer and developmental diseases.
University of California, San Francisco
Appointed in 2006
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University of California, San Francisco
Appointed in 2006
Study of mechanisms ensuring productive SRP targeting
University of California, Los Angeles
Appointed in 1985
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University of California, Los Angeles
Appointed in 1985
Cell-cell recognition
National Institute of Allergy and Infectious Diseases
Appointed in 1993
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National Institute of Allergy and Infectious Diseases
Appointed in 1993
Molecular interactions in the IL-4 receptor signaling pathway
Broad Institute
Appointed in 2017
Continual evolution of proteins in eukaryotes
New methodologies are needed to develop the next-generation of macromolecular human therapeutics that have the potential to improve our ability to treat diseases. Continuous directed evolution techniques such as phage-assisted continuous evolution (PACE) have demonstrated a transformative ability to access_x000D_
biomolecules with therapeutically relevant properties that could not have been readily accessed using conventional protein evolution methods, including improved genome editing agents, and proteases reprogrammed to cleave proteins implicated in human disease. However, PACE is greatly constrained by the requirement that it be performed in Escherichia coli, thereby precluding its application to solve important problems that require eukaryotic infrastructure, such as post-translational modification,_x000D_
chaperones that are not found in E. coli, chromatin editing or modification, subcellular localization, or organelles. I propose to design and execute a system for the continuous evolution of biomolecules in yeast, enabling access to many of these important selections. We will use this system to evolve versions of the E3 ligase MDM2 that exclusively target mutant, but not wild-type p53, for ubiquitination and degradation, demonstrating the power of eukaryotic continuous evolution to evolve proteins that are_x000D_
inaccessible to PACE, as well as generating a novel potential research tools and leads for future cancer therapeutic development.