Abstract
A method was developed to examine DNA repair within the intact cell. Ultrasoft x-rays were used to induce DNA double-strand breaks (DSBs) in defined subnuclear volumes of human fibroblasts and DNA repair was visualized at those sites. The DSBs remained in a fixed position during the initial stages of DNA repair, and the DSB repair protein hMre11 migrated to the sites of damage within 30 minutes. In contrast, hRad51, a human RecA homolog, did not localize at sites of DNA damage, a finding consistent with the distinct roles of these proteins in DNA repair.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Bromodeoxyuridine / immunology
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Bromodeoxyuridine / metabolism
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Cell Line
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Cell Nucleus / metabolism*
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DNA / metabolism*
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DNA / radiation effects
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DNA Damage*
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DNA Repair*
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DNA-Binding Proteins / metabolism
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Fibroblasts
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Fluorescein-5-isothiocyanate
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Fluorescent Antibody Technique
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Humans
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Microscopy, Confocal
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Rad51 Recombinase
Substances
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DNA-Binding Proteins
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DNA
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RAD51 protein, human
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Rad51 Recombinase
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Bromodeoxyuridine
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Fluorescein-5-isothiocyanate