Harvard University Medical School /
Colorado State University
Appointed in 1976
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Harvard University Medical School / Colorado State University
Appointed in 1976
University of Michigan
Appointed in 1964
Yale University
Appointed in 1972
Stanford University
Appointed in 1973
Princeton University
Appointed in 1990
Harvard University Medical School
Appointed in 2017
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Harvard University Medical School
Appointed in 2017
Nucleotide second messengers are crucial for development and signaling in both humans and bacteria. Nucleotide-centric pathways in human cells are targets of therapeutic interventions for cancer and diabetes, but signal regulation is complex and remains poorly understood. My work reconstructs mammalian nucleotide signaling in bacterial systems, creating the transformative opportunity to leverage bacterial genetics to uncover how these pathways are mechanistically regulated. Future findings from this work will enhance our understanding of known and previously uncharacterized cell signals in eukaryotes and prokaryotes._x000D_
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Prior to my postdoctoral work, I earned my Ph.D. in Daniel A. Portnoy’s Lab, at the University of California, Berkeley. There, I worked on essential genes and virulence regulation in the bacterial pathogen Listeria monocytogenes.
Harvard University
Appointed in 1987
University of Wisconsin, Madison
Appointed in 1965
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University of Wisconsin, Madison
Appointed in 1965
Wesleyan University
Appointed in 1982
University of Chicago
Appointed in 1965
MRC Center, University Medical School, England
Appointed in 1983
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MRC Center, University Medical School, England
Appointed in 1983
California Institute of Technology
Appointed in 1993
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California Institute of Technology
Appointed in 1993
University of Wisconsin, Madison
Appointed in 1987
Johns Hopkins University
Appointed in 1966
University of Colorado, Boulder
Appointed in 1988
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University of Colorado, Boulder
Appointed in 1988
Johns Hopkins University
Appointed in 1965
Harvard University Medical School
Appointed in 1991
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Harvard University Medical School
Appointed in 1991
Stanford University
Appointed in 1997
Salk Institute for Biological Studies
Appointed in 1974
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Salk Institute for Biological Studies
Appointed in 1974
University of Hawaii /
University of California, Davis
Appointed in 1979
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University of Hawaii / University of California, Davis
Appointed in 1979
Whitehead Institute for Biomedical Research
Appointed in 1986
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Whitehead Institute for Biomedical Research
Appointed in 1986
Harvard University Medical School
Appointed in 1972
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Harvard University Medical School
Appointed in 1972
Johns Hopkins University
Appointed in 1964
Harvard University
Appointed in 1996
University of California, Berkeley
Appointed in 1998
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University of California, Berkeley
Appointed in 1998
Yale University
Appointed in 1997
Universite de Bruxelles, Belgium
Appointed in 1960
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Universite de Bruxelles, Belgium
Appointed in 1960
Massachusetts Institute of Technology /
Columbia University
Appointed in 1984
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Massachusetts Institute of Technology / Columbia University
Appointed in 1984
University of California, Berkeley
Appointed in 2013
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University of California, Berkeley
Appointed in 2013
My research involves using isotopic labeling strategies and computational methods to enable a novel chemical glycoproteomics platform termed Isotope Targeted Glycoproteomics (IsoTaG).  Given the strong correlation of altered glycosylation patterns with malignancy, glycosylated proteins may be an information-rich subset of the proteome from which cancer biomarkers can be discovered. We employ metabolic labeling as a means to tag specific classes of glycoproteins for enrichment from human tissue samples and subsequent identification by mass spectrometry. A challenge in this endeavor is defining sites of glycosylation on peptide digests derived from such complex samples. To facilitate this effort, we invented a targeted strategy to enable the detection and identification of glycosylated peptides independent of the mass of the pendant glycan. Collectively, these tools allow us to quantitatively profile changes in protein glycosylation associated with human cancer progression and embryonic stem cell differentiation.
Harvard University Medical School
Appointed in 1984
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Harvard University Medical School
Appointed in 1984
Albert Einstein College of Medicine
Appointed in 1971
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Albert Einstein College of Medicine
Appointed in 1971
Carlsberg Laboratorium
Appointed in 1951
Massachusetts Institute of Technology
Appointed in 1966
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Massachusetts Institute of Technology
Appointed in 1966
University of Wisconsin, Madison
Appointed in 1968
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University of Wisconsin, Madison
Appointed in 1968
Yale University
Appointed in 1981
Carnegie Institute for Science
Appointed in 1993
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Carnegie Institute for Science
Appointed in 1993
Dana-Farber Cancer Institute
Appointed in 1996
Columbia University
Appointed in 2007
Rockefeller University
Appointed in 2007
Boston Children's Hospital
Appointed in 2011
Harvard University Medical School
Appointed in 2015
My research investigates the molecular mechanism of ER-associated degradation (ERAD). Using biochemical and structural tools, my study aims to understand how misfolded proteins in the ER are recognized, retro-translocated out of the ER into the cytosol, and subsequently degraded by proteasome._x000D_
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I was born and grew up in one of the big city in China, Shanghai. After receiving BS in Biology from Fudan University, my strong interest in protein biochemistry brought me overseas to pursue my PhD in molecular biochemistry and biophysics from Yale University. Working in the lab of Karin M. Reinisch, my thesis work focused on solving structures of key regulators of membrane trafficking. Currently, I am doing postdoctoral work supervised by Tom Rapoport, in whose lab I learn new skills in the exciting field of membrane biology. Outside of the lab, I like painting, and enjoy life in Boston with my family and friends.
University of California, Berkeley
Appointed in 2023
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University of California, Berkeley
Appointed in 2023
The endoplasmic reticulum (ER) is a critical organelle for maintaining protein quality control in cells; misfolded proteins are targeted for degradation through the ER-associate degradation (ERAD) pathway. Dr. Kevin Wu will study the ER-membrane bound E3 ubiquitin ligase Doa10 in Dr. Eunyong Park’s lab at the University of California, Berkeley. Doa10 is conserved from yeast to humans and identifies and targets many misfolded proteins for degradation. However, it is unclear how Doa10 recognizes a wide range of client proteins. Dr. Wu will use biochemical and structural approaches to reveal how Doa10 recognizes and processes a range of substrates, and how Doa10 cooperates with other quality control factors to maintain protein homeostasis. Protein misfolding and aggregation are associated with aging and diseases such as neurodegeneration. Thus, Wu’s studies may have implications for developing future therapies to improve protein homeostasis in human disease.
As a graduate student in Dr. James Bardwell’s lab at the University of Michigan, Wu investigated chaperone-mediated protein folding. There, he discovered that weak binding between ATP-independent chaperones enable the refolding of client proteins, whereas stronger binding hinders refolding. Dr. Wu’s background in protein refolding set him up for exploring how Doa10 E3 ubiquitin ligase recognizes unfolded protein targets.
Harvard University Medical School
Appointed in 2009
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Harvard University Medical School
Appointed in 2009
I am currently working on the connection between regulatory region sequence and function by measuring quantitative expression patterns of developmental genes in multiple Drosophila species and creating a biophysical model to interpret these data.
I have always been interested in applying methods from statistics and physics to biological problems. ¬†As an undergraduate at Rutgers University, I majored in molecular biology and statistics and did computational work in a protein NMR lab. ¬†I continued my education in Harvard University’s biophysics program, where I developed mathematical models of a wide variety of biological phenomena, including metabolic networks and protein-DNA interactions. ¬†Following an inspirational summer at the Marine Biological Laboratory¬ís physiology course, I decided to focus my postdoctoral studies on transcriptional regulation, this time combining my computational work with experiments. Outside of my research, I enjoy spending time outside — rowing, running and cross-country skiing.
Dana-Farber Cancer Institute
Appointed in 2019
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Dana-Farber Cancer Institute
Appointed in 2019
Heart failure is a common and lethal condition, yet the mechanisms by which the heart fails remains a mystery. Over the past decade, heart failure etiology has shifted from valvular heart disease and hypertension to coronary artery disease. As a result, ischemic cardiomyopathy-symptomatic left ventricular (LV) dysfunction in the setting of coronary artery disease- now accounts for nearly 70% of all heart failure causes in the United States. The exact basis of ischemic cardiomyopathy is unknown; however, identifying molecular changes in the ischemic myocardium and the generation of animal models by which these processes can be studied are an absolute necessity.
Hypoxia-inducible factor (HIF), which consists of a labile  subunit and stable  subunit, is master transcription factor that accumulates during hypoxia and activates genes whose products promote cellular survival under ischemic conditions. The HIFsubunit is regulated through prolyl hydroxylation by -ketoglutarate (KG) dependent dioxygenases known as EGLNs (also called PHDs). Acute PHD inactivation in the heart has been shown to be protective during acute cardiac ischemia in rodents, and several PHD inhibitory drugs are now in development as tissue protectant molecules. Conversely, chronic PHD inactivation or HIF stabilization itself, both predictable consequences of chronic ischemia, is sufficient to induce the hallmarks of ischemic cardiomyopathy. My work in William Kaelin’s lab has identified a new mechanism contributing to the pathogenesis of HIF-driven ischemic cardiomyopathy.
Yale University
Appointed in 1990
University of California, Berkeley /
University of California, San Diego
Appointed in 1971
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University of California, Berkeley / University of California, San Diego
Appointed in 1971
Yale University
Appointed in 2004
California Institute of Technology
Appointed in 2022
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California Institute of Technology
Appointed in 2022
By detecting molecular signatures of cancer cells, synthetic protein circuits delivered as mRNA could specifically kill cancer cells. However, a major hurdle is the inability to deliver circuits to all cancer cells in a tumor. An ideal therapy would both selectively eliminate cancer cells to which circuits are successfully delivered and trigger a broader killing effect on the surrounding tumor. Inflammatory cell death that releases immunostimulatory signals provides an ideal mechanism to achieve these two goals by directly killing on-target cancer cells, as well as indirectly killing off-target cancer cells by activating lymphocyte-mediated anti-tumor immunity. Our goal is to design protein-level circuits capable of identifying cancer cells, executing cell death, and eliciting anti-tumor immunity. We will engineer an input module that senses and amplifies oncogenic signals, design an output module that thresholds these signals and actuates inflammatory cell death, and validate the full input-output circuit using cellular and mouse cancer models. Our research will offer a novel immunotherapy concept that combines synthetic biology approaches with the immunotherapy.
Dana-Farber Cancer Institute
Appointed in 2000
University of California, San Diego
Appointed in 2010
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University of California, San Diego
Appointed in 2010
My current research is focused on understanding the neural circuit mechanism underlying the specific activation of neuronal ensembles by sensory stimuli in the mammalian cortex.
I grew up in a small town in Hunan Province, China. Both my parents are physicians.  In high school, I chanced upon the book, What Mad Pursue by Francis Crick; I was attracted to Dr. Crick’s passion for the “study of life,” and intrigued by the complexity and sophistication of biological systems. I went on to major in biology at Fudan University.
During my senior year, I became interested in neuroscience, and decided to pursuit my graduate study in the US. My graduate research at Baylor College of Medicine focused on the molecular mechanism of synaptic transmission, the process by which neurons communicate with each other.
Now I am extending my scientific interest into the synaptic mechanisms of neural circuit operation in health and disease. In my free time, I like to watch sports, play with our cats and, occasionally, help my wife in her garden.
Stanford University
Appointed in 2020
The trillions of microbes that live in and on the human body play key roles in health and disease. However, little is known about how microbes evolve in complex communities, even though this evolution can have important consequences for human health. I will study how adaptation and dispersal drive the evolution of antibiotic resistance in microbial communities, both in the human gut microbiome (in vivo) and in experimental, gut-derived microbial communities (ex vivo). First, I will track evolution in the human gut microbiome in a cohort of healthy individuals treated with ciprofloxacin. Using strain-resolved metagenomic sequencing, I will identify selective sweeps and strain replacements to determine how natural microbial communities evolve in response to a disturbance. Next, I will examine how adaptation and dispersal shape the evolution of gut-derived microbial metacommunities. These experimental metacommunities allow me to test how dispersal shapes the rates and mechanisms of adaptation in more controlled, laboratory contexts. Finally, I will study adaptation and transmission in the human gut microbiome by tracking strain transmission in cohabiting individuals before and after antibiotic treatment. This work will combine new computational and experimental approaches to shed light on how microbial communities evolve in the context of human health.