Directory

Image of Elio A. Abbondanzieri
Elio A. Abbondanzieri Jane Coffin Childs Fellow

Harvard University

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Image of Mohamad Abedi, Ph.D.
Mohamad Abedi, Ph.D. Jane Coffin Childs - HHMI Fellow

University of Washington

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Despite the tremendous efforts spent towards genetically reprogramming T cells for therapeutic purposes, the complex ex vivo procedures and costs involved in producing genetically modified lymphocytes remain major obstacles for implementing them as a standard of care in the treatment of cancer. As a JCC fellow, my goal has been to bypass these obstacles by developing a technology that combines designed protein logic with engineered viruses to target and genetically engineer specific cell populations in vivo. To achieve targeted cellular engineering in vivo, I adapted a co-localization dependent protein switch, named Co-LOCKR, that classifies cells based on their receptor expression. Upon locating cells with the correct receptor combination, Co-LOCKR presents a target peptide that guides engineered viruses to genetically modify tagged cells.

Image of Herbert T. Abelson
Herbert T. Abelson Jane Coffin Childs Fellow

Massachusetts Institute of Technology

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Image of Emma Abernathy
Emma Abernathy Jane Coffin Childs Fellow

Stanford University

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Viruses make excellent tools for studying host pathways because they have evolved ways to subvert or co-opt those pathways. I’m interested in the autophagy pathway- a highly conserved means for the cell to recycle cellular material during times of stress by promoting vesicle formation and subsequent degradation of cytoplasmic contents. Autophagy is a fascinating and broad-reaching area of research where there is still little mechanistic knowledge, but appears to be involved in many different diseases including cancer, neurodegenerative diseases, and infectious diseases.

I’m particularly interested in how viruses co-opt this pathway to promote their own replication and spread. To address the mechanisms by which viruses induce and interact with the autophagy pathway, I am using poliovirus infection in HeLa cells that have several key autophagy genes knocked out by Crispr-Cas9. This will allow me to explore how the virus interfaces with the distinct complexes of the autophagy pathway and how the virus utilizes these for replication. Using viruses to study this underlying cellular process may help uncover potential drug targets for other diseases where autophagy is implicated.

Image of Keith L. Adams
Keith L. Adams Jane Coffin Childs Fellow

Iowa State University

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Image of Paul N. Adler
Paul N. Adler Jane Coffin Childs Fellow

University of California, Irvine

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Image of Lauren C. Aguado
Lauren C. Aguado Jane Coffin Childs Fellow

Rockefeller University

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All viruses require the vast resources of a cell to complete their lifecycles, carrying with them only the tools essential for their replication that cannot be found in a host. While many viruses infect only a single or few closely related species, arboviruses constantly cycle between an insect vector and a vertebrate host. This requires that a virus be able to take advantage of two unique cellular environments while evading entirely different defense systems to do so. Many of the host factors essential for viral replication in the insect vectors remain entirely unidentified; of those that have been defined, only a subset is required in both insect and vertebrate species. Many more are utilized in only one species, leading to the hypothesis that arboviruses have found multiple ways to achieve the same ultimate goal of replication and dissemination in these dual hosts. My work seeks to understand how these disparate environments can support the replication and transmission of a single virus and how viruses can adapt to new host species.

Image of Hugo G. Aguilaniu
Hugo G. Aguilaniu Jane Coffin Childs Fellow

Salk Institute for Biological Studies

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Image of Bassem Al-Sady
Bassem Al-Sady Jane Coffin Childs Fellow

University of California, San Francisco

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Image of James L. Alderfer
James L. Alderfer Jane Coffin Childs Fellow

Johns Hopkins University

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Image of Patrick N. Allen
Patrick N. Allen Jane Coffin Childs Fellow

University of Colorado, Boulder

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Image of Gregory M. Allen
Gregory M. Allen Jane Coffin Childs Fellow

University of California, San Francisco

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Cellular therapy, exemplified by chimeric antigen receptor (CAR) T cells, is an emerging class of therapeutics that applies the principles and techniques of synthetic biology to the treatment of disease. Although promising clinical results have been obtained with CAR T cells in B Cell lymphoma and leukemia, substantial work remains to create cellular therapies that can effectively treat solid tumors. In part this is due to a lack of robust mechanisms to control spatial location of cells, which can diminish efficacy, increase toxicity and limit more sophisticated future therapeutic applications. In my research I am interested in genetically modifying T cells to create user-defined synthetic trafficking functionalities in order to promote solid tumor infiltration. In addition I am developing syngeneic mouse tumor models to synthetically control the migratory signals (chemokines) in a tumor in order to map the migration “code” a tumor uses to control the immune system. These projects have the potential to form the basis of the next generation of adoptive cellular therapies and illuminate the mechanisms that the tumor microenvironment uses to regulate the endogenous immune system.

Image of Thomas H. Alton
Thomas H. Alton Jane Coffin Childs Fellow

Stanford University

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Image of Jeanine Amacher
Jeanine Amacher Jane Coffin Childs - Frederic M. Richards Fellow

University of California, Berkeley

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Post-translational modifications regulate key interactions in signaling pathways. In protein tyrosine kinase (PTK) signaling, for example, crosstalk between phosphorylation and ubiquitylation signals is critical to proper cellular function. A phosphorylation cascade is triggered upon PTK activation; in turn, the RING-type E3 ubiquitin ligase Cbl is activated, and attenuates many of these signals via lysosomal degradation. In cancers where there are mutations in PTK signaling, this communication breaks down, leading to uncontrolled cell proliferation and poor patient prognosis.

During my postdoctoral work in Dr. John Kuriyan’s lab at UC Berkeley, I am using biochemical assays and X-ray crystallography to better understand the regulation and selectivity of Cbl with respect to its targets. Cbl has a unique activation mechanism, whereby substrate docking is followed by phosphorylation at a conserved tyrosine residue, turning Cbl “on.” I hypothesize that crosstalk between Cbl’s tyrosine kinase binding and RING domains dictates its selectivity and regulates substrate kinase activity. PTK signaling is a finely tuned product of evolution, and a greater understanding of how Cbl interacts with its substrates will unveil new possibilities for intervention.

Image of Enrique Amaya
Enrique Amaya Jane Coffin Childs Fellow

University of California, Berkeley

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Image of John E. Amoore
John E. Amoore Jane Coffin Childs Fellow

University of California, Berkeley

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Image of Margaret L.M. Anderson
Margaret L.M. Anderson Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

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Image of Karin Anderson
Karin Anderson Jane Coffin Childs Fellow

Dana-Farber Cancer Institute

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Image of Douglas A. Andres
Douglas A. Andres Jane Coffin Childs Fellow

University of Texas Southwestern Medical Center

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Image of Robin J. Andy
Robin J. Andy Jane Coffin Childs Fellow

New York University

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Image of Esther R. Angert
Esther R. Angert Jane Coffin Childs Fellow

Harvard University

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Image of Andrew V. Anzalone
Andrew V. Anzalone Jane Coffin Childs - HHMI Fellow

Broad Institute

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Image of Eftychia (Effie) Apostolou
Eftychia (Effie) Apostolou Jane Coffin Childs Fellow

Massachusetts General Hospital /
Harvard Stem Cell Institute

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My current research focuses on the molecular and epigenetic mechanisms governing the process of nuclear reprogramming of somatic cells into induced pluripotent stem cells (iPS cells). More specifically, I study how the differentiation stage of the initial somatic cell affects the efficiency of reprogramming into iPS.

I was born at Naoussa, a small town in northern Greece. I studied biology at Aristotle University of Thessaloniki and pursued my PhD on molecular ¬†biology at the medical school of the National University in Athens. While working at Dr. Dimitris Thanos¬í lab for my PhD thesis — In vivo study of the dynamics of transcriptional ¬†¬†complexes” — I became intrigued by biochemistry and familiar with molecular and cytogenetic techniques. ¬†I also published my first paper, which ¬†opened the door to Harvard University and a new world. ¬†I switched my scientific focus to this new and exciting field. I joined Dr. Konrad Hochedlinger¬ís lab and am more than happy with my choice. At the beginning of my second year, I feel so much richer in knowledge and research experience. I also enjoy life in Boston, which is an ideal city for tango dancing and hiking.”

Image of Julie E. Archer Mayo
Julie E. Archer Mayo Jane Coffin Childs Fellow

California Institute of Technology

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Image of Neali A. Armstrong
Neali A. Armstrong Jane Coffin Childs Fellow

Columbia University

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Image of Donna J. Arndt-Jovin
Donna J. Arndt-Jovin Jane Coffin Childs Fellow

Stanford University

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Image of Tal I. Arnon
Tal I. Arnon Jane Coffin Childs Fellow

California Institute of Technology

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Image of Amjad Askary
Amjad Askary Jane Coffin Childs - HHMI Fellow

California Institute of Technology

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Strong synthetic recording of cell state trajectories during development

The incredible journey from a zygote to an animal entails transition of cells from one state to another as they proliferate. Although fundamental to our understanding of development, the trajectories of single cells during these transitions have been elusive due to technical limitations. A growing body of evidence suggests that cellular heterogeneity is prevalent in biological systems. Therefore, the average behavior of cell populations cannot be reliably used to infer the trajectories of the cells they comprise. Cellular behaviors are also highly dynamic. Techniques that rely only on static snapshots lose critical information about the longitudinal dynamics and spatial context of cells.

I am interested in developing methods for recording lineage and transcriptional event histories within the genome of the cells. Recently, our group has published a CRISPR/Cas9-based method, called MEMOIR, which involves “writing” of structured mutations at defined sites in the genome, where they can be read out using multiplexed in situ hybridization. Approaches analogous to phylogenetic inference can then be used to reconstruct lineage and event histories based on the mutation patterns. I seek to improve this system and implement it in mouse embryos to study dynamics of cell state transitions in early mammalian development. This work will provide the tools and theoretical basis for reconstructing lineage trees and decorating them with dynamic gene expression information, in virtually any developmental context.

Image of Manfred Auer
Manfred Auer Jane Coffin Childs Fellow

New York University

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Image of Judith A. Austin
Judith A. Austin Jane Coffin Childs Fellow

University of California, San Francisco

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Image of Gad Avigad
Gad Avigad Jane Coffin Childs Fellow

New York University

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Image of Erika A. Bach
Erika A. Bach Jane Coffin Childs Fellow

Harvard University Medical School

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Image of Inwha Baek, Ph.D.
Inwha Baek, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

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Profound alterations in gene expression profiles occur as stem cells from normal tissue transform into cancer stem cells (or tumor-initiating cells) that are able to initiate tumor growth and propagate tumor masses. However, how the gene expression program is rewired during tumorigenesis remains elusive. My research project centers on exploring and identifying key factors that are responsible for driving the divergence of their gene expression profiles. Using in vivo mouse models and genomics and imaging approaches, I am investigating how spatiotemporal genome organization plays a role in oncogenic transcriptional reprogramming during skin squamous cell carcinoma (SCC) development. Skin SCC has emerged as a public health issue due to its increasing incidence and potential for metastasis and recurrence, particularly for the patients placed on immunosuppressive drugs. If successful, my work would further our understanding of the mechanisms underlying oncogenic transcriptional reprogramming and provide new avenues for developing new cancer therapeutics.

Image of Jihong Bai
Jihong Bai Jane Coffin Childs Fellow

Massachusetts General Hospital

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Image of Ling Bai
Ling Bai Jane Coffin Childs Fellow

University of California, San Francisco

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AgRP neurons in the arcuate nucleus of hypothalamus are exposed to plasma circulating signals and playing critical role in the regulation of feeding and homeostasis. Recently, real-time measurements of AgRP neuron activity in awake mice have revealed an unexpected rapid inhibition of these neurons by the detection and ingestion of food. These results challenge the current model for homeostatic regulation, in which AgRP neurons simply monitor circulating hormonal and nutritional signals to regulate feeding, begging the question of what physiological signals regulate AgRP neurons’ activity and generate hunger.

I propose to identify this fundamental “hunger signal” that regulates AgRP neurons through systematic experiments that combine in vivo recording with surgical, pharmacologic, genetic, and optical manipulations. I will reexamine the contribution of traditional hormonal signals, and characterize the function of different postprandial gastrointestinal stimuli in regulating AgRP neuron activity. Next, I will further identify the underlying mechanisms by examining the contribution of gastrointestinal sensory inputs as well as circulating nutrients. Together, these will aid in understanding the regulation of AgRP neuron activity and hunger, which provides a basis for the understanding of obesity as well as diverse motivated behaviors.

Image of Carl G. Baker
Carl G. Baker Jane Coffin Childs Fellow

University of California, Berkeley

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Image of Timothy S. Baker
Timothy S. Baker Jane Coffin Childs Fellow

MRC Center, University Medical School, England /
Cambridge University

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Image of Julie C. Baker
Julie C. Baker Jane Coffin Childs Fellow

University of California, Berkeley

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Image of Christa A. Baker
Christa A. Baker Jane Coffin Childs Fellow

Princeton University

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Image of Steven A. Baker
Steven A. Baker Jane Coffin Childs Fellow

Stanford University

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Aging can be viewed as the time-dependent decline in organismal function which increases the likelihood of death. How and why we age remains one of the greatest mysteries in modern biology. Interestingly, the rate of aging–and ultimately lifespan of organisms–varies greatly even within vertebrates. Among extant vertebrates, extreme longevity appears to have arisen multiple times independently, suggestive of convergent evolution. My project aims to uncover the genes and pathways that contribute to lifespan variation using comparative genomics. At present over 100 vertebrate genomes have been sequenced and are publically available. Included among these organisms are species with both remarkably short and long lifespans. I have set out to develop a computational pipeline which identifies regions that exhibit molecular convergence within the genome of species sharing a similar lifespan. I then plan to characterize these regions biochemically to determine their effects on expression, regulation, and function of the involved genes. Longer term, I will develop mutant mice harboring variants with significant effects on function to directly assess their influence on lifespan in a well-studied model of vertebrate aging.

Image of Dorairajan Balasubramanian
Dorairajan Balasubramanian Jane Coffin Childs Fellow

University of Minnesota

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Image of Michael Balls
Michael Balls Jane Coffin Childs Fellow

Reed College

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Image of Robert A. Bambara
Robert A. Bambara Jane Coffin Childs Fellow

Stanford University School of Medicine

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Image of Juan M. Barajas, Ph.D.
Juan M. Barajas, Ph.D. Jane Coffin Childs Fellow

St. Jude Children's Hospital

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Image of Karl Barber
Karl Barber Jane Coffin Childs Fellow

Brigham and Women's Hospital

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Image of Danielle Barbosa Brotto, Ph.D.
Danielle Barbosa Brotto, Ph.D. Jane Coffin Childs Fellow

University of Minnesota Twin Cities

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Human chordoma is a locally aggressive and invasive type of cancer that occurs in the bones of the skull base and spine, and it is part of a group of malignant bone and soft tissue tumors called sarcomas. It is characterized by high recurrence rates and a lack of chemotherapy response. Although studies using exome sequencing identified a few genetic alterations, the vast majority of chordomas do not appear to have a causal genetic mutation, given that the overall somatic mutation burden in chordoma is modest. Recently, the Chordoma Genome Project provided essential clues about novel genes implicated in chordoma tumorigenesis. DNA sequencing revealed that mutations in the gene encoding the lysosomal trafficking regulator protein (LYST) have a role in chordoma biology, as recurrent truncating mutations were found in 10% of tumors. Our lab has preliminary data suggesting that epigenetic regulation of LYST leads to a clinically aggressive chordoma variant, marked by reduced survival and a high rate of metastasis. Herein, this research focuses on elucidating the mechanisms of epigenetic regulation of chordoma-related genes, like LYST, by applying chromosome conformation capture and protein-DNA interaction techniques. Initial findings have shown differences in chromatin accessibility and conformation between tumor subtypes, suggesting an association with the patient’s prognosis.

Image of Stephen D. Barbour
Stephen D. Barbour Jane Coffin Childs Fellow

University of California, Berkeley

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Image of Melanie M. Barker Berkmen
Melanie M. Barker Berkmen Jane Coffin Childs Fellow

Massachusetts Institute of Technology

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Image of Jeremy Baskin
Jeremy Baskin Jane Coffin Childs - HHMI Fellow

Yale University School of Medicine

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My current research concerns the mechanisms by which cells regulate the biosynthesis of phosphoinositides, a class of lipids found on the cytosolic face of numerous membranes within the cell. In particular, I am interested in studying the metabolic interconnectedness of different classes of lipids._x000D_
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I was born and raised in Montreal, Canada in a family of artists. My parents are both classical musicians, and my younger sister is a budding actress; to this day I play classical piano as a hobby. I was drawn to chemistry in high school, and my interest in organic chemistry grew in my undergraduate years at MIT, where I received a B.S. in 2004. Midway through MIT, inspired by an advanced biochemistry class, I joined a young chemical biology lab. I continued in this area in my graduate years at UC Berkeley, in the laboratory of Carolyn Bertozzi, where my research concerned the development of chemical tools for imaging cell-surface glycans in living systems. After earning a Ph.D. in chemistry in 2009, I again switched direction, embarking on post-doctoral research in cell biology, under the supervision of Pietro De Camilli.

Image of Michael Basson
Michael Basson Jane Coffin Childs Fellow

Massachusetts Institute of Technology

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Image of David J. Bates
David J. Bates Jane Coffin Childs Fellow

Yale University

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