Directory - Jane Coffin Childs Memorial Fund

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Jun R. Huh, Ph.D. Jane Coffin Childs Fellow

New York University

Project Title: Studying the epigenetic nature of CD4 silencing in fully committed cytotoxic T cells

David WL. Hukins, Ph.D. Jane Coffin Childs Fellow

Purdue University

Project Title: Structures and interactions of intercellular polysaccharides

Eric H. Humphries, Ph.D. Jane Coffin Childs Fellow

Cancer Research UK (CRUK)

Project Title: Genetic structure of RNA tumor viruses

Ruei-Jiun Hung, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: The role of organ communications in stem cell aging

James R. Hunsley, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Translational control of cocoonase biosynthesis

John F. Hunt, Ph.D. Jane Coffin Childs Fellow

University of Texas Southwestern

Project Title: Novel membrane protein crystallization reagents

Image of M. Melissa Hunter-Ensor, Ph.D., J.D.

M. Melissa Hunter-Ensor, Ph.D., J.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Genetic analysis of neuromodulators in nematode

Robert A. Hyman, Ph.D. Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Project Title: Tumor antigens in murine myeloma cells

Maurizio Iaccarino, M.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Enzymology of nucleic acid metabolism

Kostas Iatrou, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Chorion gene organization and expression in the Silkmoth Bombyx mari

James A. Imlay, Ph.D. Jane Coffin Childs Fellow

Duke University

Project Title: Superoxide production by respiring membranes of E. coli

Jorge A. Iniguez-Lluhi, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Functional analysis of oncogene/steroid receptor

Sarah Innes-Gold, Ph.D. Merck-Jane Coffin Childs Fellow

Harvard University

Project Title: Microscopic

Cancer metastasis and immune cell migration require motile movement, meaning the cell membrane must slip relative to the cytoskeleton. Thus, membrane-cytoskeleton attachments in motile cells likely rearrange, allowing tension to propagate across the membrane. In the current literature, there are ~106-fold discrepancies in reported timescales of membrane tension propagation. I hypothesize these discrepancies reflect variability between cell types, arising from differences in membrane microstructure. I specifically hypothesize that in motile cells, transmembrane proteins are arranged to allow membrane flow, enabling rapid tension equilibration, while non-motile cell membranes are structured to impede tension propagation.

I will directly measure tension propagation timescales in motile and non-motile cells and simultaneously characterize the arrangement of cytoskeleton-anchored transmembrane proteins. I will use optical tweezers to stretch membrane tethers, perturbing and measuring tension. I will visualize immobile transmembrane proteins with targeted photochemical labeling and high-resolution fluorescence imaging, revealing how transmembrane protein arrangement regulates membrane fluidity, and how cancer cells might exploit this to metastasize

Arthur A. Iodice, Ph.D. Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: Intermediary metabolism of bacteria - biochemical techniques including the use of isotopic tracer material

Javier E. Irazoqui, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Dissection of innate immunity in C elegans

Keith P. Ireton, Ph.D. Jane Coffin Childs Fellow

Institut Pasteur

Project Title: Role for phosphoinositide 3-kinase in bacterial invasion

Vivian F. Irish, Ph.D. Jane Coffin Childs Fellow

University of Cambridge, England /
Yale University

Project Title: Genetic and molecular basis of positional specification

Ralph R. Isberg, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: DNA sequencing

Hannah L. Itell, Ph.D. Jane Coffin Childs Fellow

Vanderbilt University Medical Center

Project Title: Defining the targets of the antibody response to natural Oropouche virus infection

Dr. Hannah Itell’s passion for understanding the “ever-evolving virus-host arms race” started during her undergraduate global health studies in India, South Africa, and Brazil. Seeing the impact of viral infection on individuals, families, communities, and entire countries, motivated Itell to dedicate her research career to preventing viral transmission.

In her graduate research in Dr. Julie Overbaugh’s lab at the Fred Hutchinson Cancer Center, Itell focused on identifying human traits that limit HIV severity. She discovered that many virus-fighting genes seen in lab-grown cells function differently than real human immune cells,, demonstrating that common lab models may not reflect what really happens in the body. Next, she identified a gene that regulates a pattern in HIV transmission that was not previously understood.

Now as a Fellow in Dr. Ivelin Georgiev’s lab at Vanderbilt, Itell has switched her focus to the Oropouche virus which is endemic to Brazil.There are currently no vaccines or specific treatments available to prevent or treat infection. Itell will find out how many virus types can be blocked by antibodies and where on the virus the antibodies attach. Itell’s efforts will provide fundamental knowledge about host response to Oropouche virus and directly inform rational vaccine design in the development of antibody therapeutics.

Shigeki Iwase, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Roles of a histone demethylase SMCX in neuronal function

Anthony S. Jack, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Structure of spherical viruses

Joseph W. Jack, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Molecular basis of transvection in Drosophila

Allan S. Jacobson, Ph.D. Jane Coffin Childs Fellow

University of Massachusetts Chan Medical School

Project Title: Regulation of slime mold mRNA synthesis

Deepti Jain, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Mechanism of transcription activation

Aakanksha Jain, Ph.D. Jane Coffin Childs Fellow

Boston Children's Hospital

Project Title: Somatosensory control of barrier tissue immunity

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‚Äì the nociceptors ‚Äì 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.

Rishi Jajoo, Ph.D. Jane Coffin Childs Fellow

University of California, Irvine

Project Title: Quantitative mito proteomics via non-canonical amino acid incorporation

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.

Edward B. Jakobovits, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Construction of hormone modulated transformed cells

Sirpa T. Jalkanan, M.D., Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Homing mechanisms of normal and malignant lymphocytes

John R. James, Ph.D. HHMI-Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Defining the role of the actin cytoskeleton in plasma membrane organization during T-cell activation

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.

Philip A. James, Ph.D. Jane Coffin Childs Fellow

University of Wisconsin, Madison

Project Title: Multiple protein tyrosine phosphatase genes from the yeast S. cerevisiae

Milan A. Jamrich, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Gene expression

Claudia Y. Janda, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Elucidating the molecular basis of canonical Wnt signaling activation and inhibition at the cell surface

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.

Maria Jasin, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Homologous recombination in mammalian cells

Khashayar Javaherian, Ph.D. Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: Interactions of proteins with nucleic acids

Jamshid Javid , M.D. Jane Coffin Childs Fellow

Montefiore Hospital

Project Title: Metabolism of hemoglobin

Warren Jelinek, Ph.D. Jane Coffin Childs Fellow

Columbia University

Project Title: Incorporation of adenovirus into the host DNA of transformed cells

Peter GN. Jeppesen, Ph.D. Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Project Title: SV40 DNA and SV40 messenger RNA

Wenyan Jiang, Ph.D. Simons Foundation-Jane Coffin Childs Fellow

Columbia University

Project Title: Microbial adaptation to extreme environments facilitated by CRISPR-Cas

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.

Yishi Jin, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Neuronal cell differentiation

Randall S. Johnson, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: AP-1 factors in mouse models of tumorigenesis

Tracy L. Johnson, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Yeast mRNA splicing

Alyssa E. Johnson, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Mechanisms of VCP-mediated cellular degeneration

Zachary L. Johnson, Ph.D. HHMI-Jane Coffin Childs Fellow

Rockefeller University

Project Title: Structural and mechanistic studies of multidrug resistance mediated by MRP1

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.

Edward M. Johnson, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Chromosome structure

James C. Johnson, Ph.D. Jane Coffin Childs Fellow

Albert Einstein College of Medicine

Project Title: Role of protein phosphorylation in tumor virus infection

Robert J. Johnston, Ph.D. Jane Coffin Childs Fellow

New York University

Project Title: Stochastic fate choice generating the retinal mosaic

Y'Vonne R. Jones-Brown, Ph.D. Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: Yeast mating pheromones: their mechanism of action

Paul C. Jorgensen, Ph.D., J.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Vertebrate growth control in a developmental context

Leemor Joshua-Tor, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: GAL6-A DNA-binding protease

Katherine I. Joubin, Ph.D. Jane Coffin Childs Fellow

New York University

Project Title: Role of nodal signaling during gastrulation

Nicholas Jourjine, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Genetic and neural basis of natural variation in infant vocalization

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.