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Amy M. Furda

Researcher at University of Pittsburgh

Publications -  6
Citations -  756

Amy M. Furda is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 5, co-authored 6 publications receiving 680 citations.

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Book ChapterDOI

Quantitative PCR-based measurement of nuclear and mitochondrial DNA damage and repair in mammalian cells.

TL;DR: A gene-specific quantitative PCR (QPCR)-based assay for the measurement of DNA damage, using amplification of long DNA targets, which has been used extensively to measure the integrity of both nuclear and mitochondrial genomes exposed to different genotoxins.
Journal ArticleDOI

Crucial role for DNA ligase III in mitochondria but not in Xrcc1-dependent repair

TL;DR: The results establish a role for Lig3 in mitochondria, but distinguish it from its interacting protein Xrcc1, which can be circumvented by targeting Lig1 to the mitochondria or expressing Chlorella virus DNA ligase, the minimal eukaryal nick-sealing enzyme, or Escherichia coli LigA, an NAD-dependent ligase.
Journal ArticleDOI

Oxidants and not alkylating agents induce rapid mtDNA loss and mitochondrial dysfunction.

TL;DR: It is suggested that persistent mtDNA damage is not sufficient to cause mitochondrial dysfunction and levels of mitochondrial- and nuclear-encoded proteins using antibody analysis and a pharmacologic profile of mitochondria using the Seahorse Extracellular Flux Analyzer suggest this.
Book ChapterDOI

Analysis of DNA damage and repair in nuclear and mitochondrial DNA of animal cells using quantitative PCR.

TL;DR: This chapter was written as a guide to using the long-amplicon quantitative PCR (QPCR) assay for the measurement of DNA damage in mammalian as well as nonmammalian species such as Caenorhabditis elegans, Drosophila melanogaster, and two species of fish.
Journal ArticleDOI

Functional characterization of the RAD51D E233G genetic variant

TL;DR: The findings suggest that the E233G variant affects RAD51D functions and protein interactions and increases cellular chemoresistance, the first to analyze the functional effects of a clinically relevant RAD51d amino acid substitution.