Directory

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

University of Oregon

Appointed in 2003

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Image of Bryce Carey
Bryce Carey Jane Coffin Childs - HHMI Fellow

Rockefeller University

Appointed in 2012

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Image of Philip L.M. Carl
Philip L.M. Carl Jane Coffin Childs Fellow

King's College, London

Appointed in 1968

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Image of Marian B. Carlson
Marian B. Carlson Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1978

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Image of Gordon G. Carmichael
Gordon G. Carmichael Jane Coffin Childs Fellow

Swiss Institute of Experimental Cancer Research, Switzerland

Appointed in 1975

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Image of James M. Carothers
James M. Carothers Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2006

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Image of Agamemnon J. Carpousis
Agamemnon J. Carpousis Jane Coffin Childs Fellow

University of California, Santa Barbara

Appointed in 1983

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Image of Dana Carroll
Dana Carroll Jane Coffin Childs Fellow

Beatson Institute for Cancer Research, Scotland

Appointed in 1970

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Image of Andrew P. Carter
Andrew P. Carter Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2003

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Image of Ava Carter
Ava Carter Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2020

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Image of Edward A. Carusi
Edward A. Carusi Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 1958

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Image of Pedro S. Carvalho
Pedro S. Carvalho Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2005

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Image of Jason M. Casolari
Jason M. Casolari Jane Coffin Childs Fellow

Stanford University School of Medicine

Appointed in 2006

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Image of Pau Castel
Pau Castel Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2017

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Image of Joseph Castellano
Joseph Castellano Jane Coffin Childs - Simons Foundation Fellow

Stanford University School of Medicine

Appointed in 2013

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During my Ph.D. studies at Washington University, I worked with David Holtzman to show that ApoE e4 may increase Alzheimer’s disease risk by impairing Ab clearance from the brain, thus shifting the onset of its accumulation. My interest in neurodegeneration and aging motivated me to understand factors that regulate aging and brain health in unconventional ways. My project as a Jane Coffin Childs fellow in Tony Wyss-Coray’s laboratory has been to elucidate a novel systemic-neurogenic communication mechanism that appears to be disrupted in the context of brain irradiation therapy. Specifically, I am investigating the role of immune signaling molecules in mediating the neurogenic and cognitive dysfunction observed in the post-irradiation syndrome in pediatric brain cancer patients. Additionally, I am actively pursuing whether related blood-borne signaling molecules in young plasma may be sufficient to ameliorate age-related decreases in cognition and synaptic plasticity. To examine these complex mechanisms, I am leveraging various physiological methods, including plasma transfer and parabiosis.

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

Yale University /
University of California, Berkeley

Appointed in 1974

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Image of Kate Cavanaugh, Ph.D.
Kate Cavanaugh, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2021

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Infertility represents a significant societal burden, as nearly 60% of human pregnancies fail before the embryo implants into the uterus. These miscarriages become more prevalent as women age above 35 years. But implantation remains a black box within development because it occurs within the mother’s body, so progress revealing its physical mechanisms is lagging. Early in preimplantation sages, primitive placental lineages must be specified for faithful implantation. Driving these lineage commitments are subcellular mechanical forces that transduce expression of downstream fate determinants for specification and ultimate invasion of placental tissues. However, in mammalian embryos of aged mothers, embryos display poor developmental health with decreased placental structures owing to impaired implantation. We hypothesize that these pathologies may stem from either early defects in tissue specification or later mechanical uterine invasion, both of which could give rise to age-related spontaneous abortions. This proposal therefore seeks to understand how the early cell biological and biophysical mechanisms are altered in the embryo with advanced maternal age, and how these mechanisms can be tuned to rejuvenate “aged” embryos to rescue developmental potential. Working in embryos of aged mice, we will combine approaches from cell and developmental biology, biophysics, and synthetic biology to ask: (1) Does maternal aging decouple the embryo’s upstream mechanics from downstream signal transduction during placental fate acquisition? (2) Is the logic of signal transduction for placental fate determinants altered via maternal aging? and (3) Do these age-related mechanisms together promote defective mechanical invasion during uterine implantation? Bridging these disparate scientific spheres will be critical in understanding infertility and improving female reproductive longevity.

Image of Pelin M. Cayirlioglu
Pelin M. Cayirlioglu Jane Coffin Childs Fellow

University of California, Los Angeles

Appointed in 2003

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Image of Carol L.M. Cech
Carol L.M. Cech Jane Coffin Childs Fellow

Harvard University

Appointed in 1975

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Image of Constance L. Cepko
Constance L. Cepko Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1982

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Image of Heriberto D. Cerutti
Heriberto D. Cerutti Jane Coffin Childs Fellow

Duke University

Appointed in 1992

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Image of QueeLim Ch'ng
QueeLim Ch'ng Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2001

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Image of Yunrong Chai
Yunrong Chai Jane Coffin Childs Fellow

Harvard University

Appointed in 2006

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Image of Debrabrata Chakravarti
Debrabrata Chakravarti Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Appointed in 1994

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Image of Glenn H. Chambliss
Glenn H. Chambliss Jane Coffin Childs Fellow

Universite de Paris, France

Appointed in 1971

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Image of Wendy C. Champness
Wendy C. Champness Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1982

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Image of Phillip C. Chan
Phillip C. Chan Jane Coffin Childs Fellow

Insitut for Biochemie, Max-Planck-Institut

Appointed in 1959

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Image of Russell K. Chan
Russell K. Chan Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1974

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Image of David Chan
David Chan Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 1996

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Image of Vikram Chandra, Ph.D.
Vikram Chandra, Ph.D. Jane Coffin Childs Fellow

Harvard University

Appointed in 2021

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How animal brains evolved the capacity for sophisticated computation is not well understood. One major facet of this problem is the evolution of chemosensation. Chemosensation is the primary sense of most animals, and involves complex neural computations. We do not know how this sense evolved, or how most animals – which are aquatic invertebrates – perform chemosensation. I am studying chemosensation in an acoel worm, an aquatic invertebrate that by virtue of its phylogenetic position as the likely outgroup to all other animals with central nervous systems, retains some primitive features of early central nervous systems. Acoels nonetheless perform sophisticated behavior that requires complex chemosensory processing, but how their brains and chemosensors work is unknown. Using a combination of automated behavioral tracking, transgenics, and neural activity imaging, I aim to understand the logic of chemosensory processing in a tractable acoel worm. Through comparisons with known chemosensory mechanisms of other animals, this will shed light on how complex chemosensory systems evolved. This project will also establish experimental approaches for the future study of neural computations and behavior in acoel worms and other aquatic invertebrates.

Image of Christopher J. Chang
Christopher J. Chang Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2002

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Image of Michelle Chia-yu Chang
Michelle Chia-yu Chang Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2005

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Image of Pamela Chang
Pamela Chang Jane Coffin Childs Fellow

Yale University

Appointed in 2011

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Image of Luke Chao
Luke Chao Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2012

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Image of David D. Chaplin
David D. Chaplin Jane Coffin Childs Fellow

Harvard University

Appointed in 1982

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Image of Fabienne C. Charles De La Brousse
Fabienne C. Charles De La Brousse Jane Coffin Childs Fellow

Carnegie Institute for Science

Appointed in 1991

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Image of Maureen J. J. Charron
Maureen J. J. Charron Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 1987

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Image of Lawrence A. Chasin
Lawrence A. Chasin Jane Coffin Childs Fellow

Centre Nationale de la Recherche Scientifique, France

Appointed in 1966

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Image of Iain M. Cheeseman
Iain M. Cheeseman Jane Coffin Childs Fellow - Ludwig Institute

University of California, San Diego

Appointed in 2003

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Image of Shepley S.C. Chen
Shepley S.C. Chen Jane Coffin Childs Fellow

Michigan State University

Appointed in 1965

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Image of Ji H. Chen
Ji H. Chen Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1972

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Image of Yen-Chih J. Chen
Yen-Chih J. Chen Jane Coffin Childs Fellow

Scripps Research Institute

Appointed in 1989

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Image of Alice E. Chen
Alice E. Chen Jane Coffin Childs - Merck Fellow

Harvard University

Appointed in 2005

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Image of Jichao Chen
Jichao Chen Jane Coffin Childs Fellow

Stanford University

Appointed in 2007

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Image of Xi Chen
Xi Chen Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2012

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Image of Jia-Yun Chen
Jia-Yun Chen Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2014

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Image of Yi Chen
Yi Chen Jane Coffin Childs Fellow

Dana-Farber Cancer Institute

Appointed in 2015

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My current research focuses on the molecular mechanisms underlying adipose tissue development and metabolism.  In particular, I use genetic and biochemical approaches to identify the molecular differences between the energy-storing white fat and energy-dissipating brown/beige fat in the hope of using those differences to help design therapeutic strategies for the prevention and treatment of obesity._x000D_
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Brown and beige fat dissipates energy as heat in a process known as non-shivering thermogenesis. The transcriptional regulator Prdm16 was previously identified to facilitate thermogenesis; however, its relevant target genes remain incompletely known. Through ChIP-Seq and RNA-Seq, we have identified a number of potential Prdm16 targets. Among those, I focus on delineating the functions of a rectifying potassium channel Kcnk3 in thermogenesis. Kcnk3 is known to set the plasma membrane potential by generating potassium currents in neurons. I hypothesize that Kcnk3 sets the appropriate membrane potential in thermogenic adipocytes, which may be important for thermogenesis. I will test this hypothesis using fat-specific Kcnk3 knockout mice.

Image of Feng Chen
Feng Chen Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2015

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Image of Yu-Chan Chen
Yu-Chan Chen Jane Coffin Childs Fellow

Stanford University

Appointed in 2016

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Proteostasis is a central mechanism to regulate the health of the cellular proteome. Proteostasis dysfunction has been directly implicated­­ in age-related diseases, including cancer. A central but very poorly understood component of proteostasis network is the eukaryotic chaperonin, TRiC/CCT. TRiC is an essential chaperone that assists folding and assembly of many proteins fundamentally important to cancer, including the tumor suppressors p53, VHL, telomerase as well as other cell cycle regulators. It is, therefore, not surprising that mis-regulation of TRiC is also linked to numerous pathological conditions. Indeed, several TRiC subunits are highly up-regulated in cancer, and their up-regulation is linked to poor prognosis. The paucity of structural and mechanistic knowledge on this complex has hindered the development of therapeutic strategies targeting TRiC. Therefore, my research in the Frydman lab focuses on closing this gap by defining the molecular basis of human TRiC to fold the key disease-linked proteins. I am interested in combining biochemical and structural methods to elucidate the underlying principles by which TRiC recognizes and folds proteins. I anticipate the result of this work will provide mechanistic insights relevant to human diseases.

Image of Jin Chen
Jin Chen Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2016

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Long non-coding RNAs (lncRNAs) have recently emerged as key functional molecules in gene regulation, with increasing evidence pointing to a role for lncRNAs in human diseases such as cancer. While the importance of a subset of nuclear lncRNAs in epigenetic and transcriptional gene regulation is well established, lncRNAs are also found in the cytoplasm and may function in different cytoplasmic processes including translational control. In particular, lncRNAs may regulate the translation of other transcripts; or, they may be associated with ribosomes and translated to produce short regulatory “micropeptides”. However, studying the roles for lncRNAs in translation has been hindered by the lack of high-throughput methods to systematically identify lncRNA candidates and probe how lncRNAs act globally to impact translation. Here, I propose a research program that uses a repertoire of genome-wide techniques, combining CRISPR interference and ribosome profiling, to provide fundamental insights into the novel role of lncRNAs in translational control.

Image of Jingxun Chen
Jingxun Chen Jane Coffin Childs Fellow

Stanford University

Appointed in 2020

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Reproductive aging is a global challenge. Older men and women face fertility loss and a higher chance of having children with genetic disorders. Currently, we lack a detailed molecular understanding of what causes reproductive aging in vertebrates. I am developing an emerging short-lived model system, the African killifish, to study vertebrate reproductive aging. The lifespan of this organism is 4 times shorter than mice and 7 times shorter than zebrafish. I will combine my graduate training (gamete biology) with the expertise of the Brunet Lab (killifish and aging) to probe the molecular basis of age-dependent fertility decline in the killifish and identify potential targets for therapeutic intervention. These studies will shed light on methods to protect or rejuvenate the germline from aging, which can have a profound impact on human fertility.