S
Stuart Linn
Researcher at University of California, Berkeley
Publications - 129
Citations - 14525
Stuart Linn is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: DNA & DNA polymerase. The author has an hindex of 59, co-authored 129 publications receiving 13955 citations. Previous affiliations of Stuart Linn include University of California, San Francisco.
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Journal ArticleDOI
Molecular Mechanisms of Mammalian DNA Repair and the DNA Damage Checkpoints
TL;DR: The molecular mechanisms of DNA repair and the DNA damage checkpoints in mammalian cells are analyzed and apoptosis, which eliminates heavily damaged or seriously deregulated cells, is analyzed.
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Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro.
TL;DR: An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide.
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Formation, Prevention, and Repair of DNA Damage by Iron/Hydrogen Peroxide
Ernst S. Henle,Stuart Linn +1 more
TL;DR: The cytotoxic effects of O2 .
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Mutagenesis and stress responses induced in Escherichia coli by hydrogen peroxide
James A. Imlay,Stuart Linn +1 more
TL;DR: Analysis of the sensitivities of mutants that are deficient in individual SOS-regulated functions suggested that the SOS-mediated protection is due to the enhanced synthesis of recA protein, which is rate limiting for recombinational DNA repair.
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Bimodal pattern of killing of DNA-repair-defective or anoxically grown Escherichia coli by hydrogen peroxide.
James A. Imlay,Stuart Linn +1 more
TL;DR: Two modes of killing of Escherichia coli K-12 by hydrogen peroxide can be distinguished: mode-one killing required active metabolism during the H2O2 challenge, and it resulted in sfiA-independent filamentation of both cells which survived and those which were killed by the challenge; and mode-two killing did not require active metabolism, and killed cells did not filament, although survivors demonstrated a dose-dependent growth lag.