Michael A Lodato, Ph.D.

Affiliations: 
2019- Molecular, Cell, and Cancer Biology University of Massachusetts Medical School, Worcester, MA, United States 
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"Michael Lodato"
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Parents

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Rudolf Jaenisch grad student 2007-2013 MIT
Chris A. Walsh post-doc 2013-2019 Children's Hospital Boston

Collaborators

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Michael B. Miller collaborator 2017- (Chemistry Tree)
Mollie Woodworth collaborator 2013-2016 Children's Hospital Boston
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Publications

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Lodato MA, Ziegenfuss JS. (2022) The two faces of DNA oxidation in genomic and functional mosaicism during aging in human neurons. Frontiers in Aging. 3: 991460
Kim J, Huang AY, Johnson SL, et al. (2022) Prevalence and mechanisms of somatic deletions in single human neurons during normal aging and in DNA repair disorders. Nature Communications. 13: 5918
Luquette LJ, Miller MB, Zhou Z, et al. (2022) Single-cell genome sequencing of human neurons identifies somatic point mutation and indel enrichment in regulatory elements. Nature Genetics
Choudhury S, Huang AY, Kim J, et al. (2022) Somatic mutations in single human cardiomyocytes reveal age-associated DNA damage and widespread oxidative genotoxicity. Nature Aging. 2: 714-725
Bae T, Fasching L, Wang Y, et al. (2022) Analysis of somatic mutations in 131 human brains reveals aging-associated hypermutability. Science (New York, N.Y.). 377: 511-517
Miller MB, Huang AY, Kim J, et al. (2022) Somatic genomic changes in single Alzheimer's disease neurons. Nature
Bourseguin J, Cheng W, Talbot E, et al. (2022) Persistent DNA damage associated with ATM kinase deficiency promotes microglial dysfunction. Nucleic Acids Research
Kim J, Zhao B, Huang AY, et al. (2020) APP gene copy number changes reflect exogenous contamination. Nature. 584: E20-E28
Lodato MA, Walsh CA. (2019) Corrigendum: Genome aging: somatic mutation in the brain links age-related decline with disease and nominates pathogenic mechanisms. Human Molecular Genetics
Lodato MA, Walsh CA. (2019) Genome aging: somatic mutation in the brain links age-related decline with disease and nominates pathogenic mechanisms. Human Molecular Genetics
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