Dennis Kim, MD, PhD
Chief, Division of Infectious Diseases; Senior Physician in Pediatrics, Division of Infectious Diseases
R. Cannon Eley, MD Professor of Pediatrics, Harvard Medical School
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Dennis Kim, MD, PhD
Chief, Division of Infectious Diseases; Senior Physician in Pediatrics, Division of Infectious Diseases
R. Cannon Eley, MD Professor of Pediatrics, Harvard Medical School
Medical Services
Languages
English
Education
Medical School
Harvard Medical School
1997
Boston
MA
Internship
Brigham & Women's Hospital
1998
Boston
MA
Residency
Brigham & Women's Hospital
1999
Boston
MA
Fellowship
Brigham & Women's Hospital/Massachusetts General Hospital
2003
Boston
MA
Certifications
American Board of Internal Medicine (Infectious Diseases)
Professional History
Dennis Kim, M.D., Ph.D., is Chief of the Division of Infectious Diseases at Boston Children’s Hospital. He received his undergraduate education at the University of California at Berkeley, and his medical and graduate degrees at Harvard Medical School. He completed his internship and residency in Internal Medicine at the Brigham and Women’s Hospital, and subspecialty training in Infectious Diseases from the combined program at the Massachusetts General Hospital and Brigham and Women’s Hospital. He is a Fellow of the Infectious Disease Society of America. Prior to assuming his current position at Boston Children’s Hospital, for thirteen years Dr. Kim served as a Professor in the Department of Biology at the Massachusetts Institute of Technology, while also maintaining clinical attending responsibilities in Infectious Diseases at the Massachusetts General Hospital.
Approach to Care
I came to Boston Children’s Hospital with a commitment to promoting the health and well-being of children by advancing the clinical and research missions of the Division of Infectious Diseases.
Publications
Bacteria are a major determinant of Orsay virus transmission and infection in Caenorhabditis elegans. View Abstract
Genetic variants that modify neuroendocrine gene expression and foraging behavior of C. elegans. View Abstract
Bacteria Are a Major Determinant of Orsay Virus Transmission and Infection in Caenorhabditis elegans. View Abstract
Neuroendocrine gene expression coupling of interoceptive bacterial food cues to foraging behavior of C. elegans. View Abstract
Germline mitotic quiescence and cell death are induced in Caenorhabditis elegans by exposure to pathogenic Pseudomonas aeruginosa. View Abstract
Neuroendocrine Gene Expression Coupling of Interoceptive Bacterial Food Cues to Foraging Behavior of C. elegans. View Abstract
Genetic Variants That Modify the Neuroendocrine Regulation of Foraging Behavior in C. elegans. View Abstract
Germline mitotic quiescence and programmed cell death are induced in C. elegans by exposure to pathogenic P. aeruginosa. View Abstract
Neuronal KGB-1 JNK MAPK signaling regulates the dauer developmental decision in response to environmental stress in Caenorhabditis elegans. View Abstract
Host-microbe interactions and the behavior of Caenorhabditis elegans. View Abstract
Immediate activation of chemosensory neuron gene expression by bacterial metabolites is selectively induced by distinct cyclic GMP-dependent pathways in Caenorhabditis elegans. View Abstract
Population Density Modulates the Duration of Reproduction of C. elegans. View Abstract
Global transcriptional regulation of innate immunity by ATF-7 in C. elegans. View Abstract
Bacterial Siderophores Promote Animal Host Iron Acquisition and Growth. View Abstract
Endoplasmic Reticulum Homeostasis Is Modulated by the Forkhead Transcription Factor FKH-9 During Infection of Caenorhabditis elegans. View Abstract
Signaling in the innate immune response. View Abstract
PDF-1 neuropeptide signaling regulates sexually dimorphic gene expression in shared sensory neurons of C. elegans. View Abstract
Molecular Determinants of the Regulation of Development and Metabolism by Neuronal eIF2a Phosphorylation in Caenorhabditis elegans. View Abstract
Sexually dimorphic control of gene expression in sensory neurons regulates decision-making behavior in C. elegans. View Abstract
Age-Dependent Neuroendocrine Signaling from Sensory Neurons Modulates the Effect of Dietary Restriction on Longevity of Caenorhabditis elegans. View Abstract
Mutations in Nonessential eIF3k and eIF3l Genes Confer Lifespan Extension and Enhanced Resistance to ER Stress in Caenorhabditis elegans. View Abstract
IRE1 Sulfenylation by Reactive Oxygen Species Coordinates Cellular Stress Signaling. View Abstract
Inhibition of Lithium-Sensitive Phosphatase BPNT-1 Causes Selective Neuronal Dysfunction in C. elegans. View Abstract
Signal Transduction: A Different Kind of Toll Is in the BAG. View Abstract
Tissue expression pattern of PMK-2 p38 MAPK is established by the miR-58 family in C. elegans. View Abstract
Chemosensation of bacterial secondary metabolites modulates neuroendocrine signaling and behavior of C. elegans. View Abstract
Behavioral avoidance of pathogenic bacteria by Caenorhabditis elegans. View Abstract
The unfolded protein response in a pair of sensory neurons promotes entry of C. elegans into dauer diapause. View Abstract
Bacteria and the aging and longevity of Caenorhabditis elegans. View Abstract
Physiological IRE-1-XBP-1 and PEK-1 signaling in Caenorhabditis elegans larval development and immunity. View Abstract
Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour. View Abstract
Caenorhabditis elegans NPR-1-mediated behaviors are suppressed in the presence of mucoid bacteria. View Abstract
A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans. View Abstract
Phosphorylation of the conserved transcription factor ATF-7 by PMK-1 p38 MAPK regulates innate immunity in Caenorhabditis elegans. View Abstract
An essential role for XBP-1 in host protection against immune activation in C. elegans. View Abstract
Tissue-specific activities of an immune signaling module regulate physiological responses to pathogenic and nutritional bacteria in C. elegans. View Abstract
The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response. View Abstract
A polymorphism in npr-1 is a behavioral determinant of pathogen susceptibility in C. elegans. View Abstract
Studying host-pathogen interactions and innate immunity in Caenorhabditis elegans. View Abstract
Transcriptional responses to pathogens in Caenorhabditis elegans. View Abstract
p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. View Abstract
Evolutionary perspectives on innate immunity from the study of Caenorhabditis elegans. View Abstract
Integration of Caenorhabditis elegans MAPK pathways mediating immunity and stress resistance by MEK-1 MAPK kinase and VHP-1 MAPK phosphatase. View Abstract
The Caenorhabditis elegans MAPK phosphatase VHP-1 mediates a novel JNK-like signaling pathway in stress response. View Abstract
Requirement for a conserved Toll/interleukin-1 resistance domain protein in the Caenorhabditis elegans immune response. View Abstract
Long-lived C. elegans daf-2 mutants are resistant to bacterial pathogens. View Abstract
A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. View Abstract
Locations