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Tom Maniatis

Tom Maniatis

· Professor of Biochemistry and Molecular Biophysics

Columbia University · Biochemistry and Molecular Biophysics

Active 1968–2025

h-index162
Citations246.7k
Papers39649 last 5y
Funding$133.0M1 active

Academic metrics are sourced from OpenAlex and public funding records; values may differ from Google Scholar.

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About

Tom Maniatis, PhD, is the Isidore S. Edelman Professor of Biochemistry at Columbia University Irving Medical Center, affiliated with the Mortimer B. Zuckerman Mind Brain Behavior Institute. He is renowned for pioneering the development of gene cloning technology and its application to basic research and biotechnology, coauthoring the definitive laboratory manual on Molecular Cloning. His research has led to fundamental advances in understanding gene regulation, RNA splicing, innate immunity signaling pathways, single cell diversity in the nervous system, and neurodegenerative disease mechanisms. Dr. Maniatis received his B.A. and M.S. degrees from the University of Colorado in chemistry and biology, and his Ph.D. in molecular biology from Vanderbilt University. He completed postdoctoral studies at Harvard University and the Laboratory of Molecular Biology in Cambridge, England. His academic career includes positions at the California Institute of Technology and Harvard University. Currently, he serves as the Director of the Columbia University Precision Medicine Initiative, a member of the Executive Committee of the Zuckerman Mind Brain Behavior Institute, and the Principal Investigator of the Maniatis Lab. His research over the past decade has focused on disease mechanisms of ALS, utilizing human genetic, stem cell, and animal model approaches, as well as studying the structure and function of the clustered protocadherin genes, with investigations into motor and affective…

Research topics

  • Medicine
  • Immunology
  • Internal medicine
  • Biology
  • Virology
  • Pathology
  • Environmental health
  • Genetics

Selected publications

  • Autoantibodies against type I IFNs in patients with life-threatening COVID-19

    Science · 2020 · 2828 citations

    Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type…

  • Inborn errors of type I IFN immunity in patients with life-threatening COVID-19

    Science · 2020 · 2384 citations

    Clinical outcome upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ranges from silent infection to lethal coronavirus disease 2019 (COVID-19). We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern Toll-like receptor 3 (TLR3)- and interferon regulatory factor 7 (IRF7)-dependent type I interferon (IFN) immunity to influenza virus in 659 patients with life-threatening COVID-19 pneumonia relative to 534…

  • Human genetic and immunological determinants of critical COVID-19 pneumonia

    Nature · 2022 · 388 citations

  • The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

    Proceedings of the National Academy of Sciences · 2022 · 188 citations

    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection fatality rate (IFR) doubles with every 5 y of age from childhood onward. Circulating autoantibodies neutralizing IFN-α, IFN-ω, and/or IFN-β are found in ∼20% of deceased patients across age groups, and in ∼1% of individuals aged <70 y and in >4% of those >70 y old in the general population. With a sample of 1,261 unvaccinated deceased patients and 34,159 individuals of the general population sampled before the pandemic, we es…

  • SARS-CoV-2–related MIS-C: A key to the viral and genetic causes of Kawasaki disease?

    The Journal of Experimental Medicine · 2021 · 149 citations

    Multisystem inflammatory syndrome in children (MIS-C) emerged in April 2020 in communities with high COVID-19 rates. This new condition is heterogenous but resembles Kawasaki disease (KD), a well-known but poorly understood and clinically heterogenous pediatric inflammatory condition for which weak associations have been found with a myriad of viral illnesses. Epidemiological data clearly indicate that SARS-CoV-2 is the trigger for MIS-C, which typically occurs about 1 mo after infection. These…

Recent grants

Frequent coauthors

  • Yu Zhang

    207 shared
  • Jean‐Laurent Casanova

    Université Paris Cité

    150 shared
  • Qian Zhang

    Inserm

    137 shared
  • Laurent Abel

    Université Paris Cité

    124 shared
  • YL Lau

    University of Hong Kong

    104 shared
  • Peng Zhang

    Zhejiang Hospital

    92 shared
  • Emmanuelle Jouanguy

    Hospital for Sick Children

    74 shared
  • Laurent Rénia

    Agency for Science, Technology and Research

    73 shared

Education

  • B.A., Chemistry

    University of Colorado

  • M.S., Biology

    University of Colorado

  • Ph.D., Molecular Biology

    Vanderbilt University

Awards & honors

  • Eli Lilly Award in Microbiology and Immunology
  • The Richard Lounsbery Award for Biology and Medicine
  • 2012 Lasker-Koshland Special Achievement Award in Medical Sc…

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