DNA Repair and Mutagenesis

By E. Friedberg, G. Walker, W. Siede. 2006

3,371 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/69a1ae800d2a3f7ad477a08d9a3eef04133be63d

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Citations in the corpus

Alkylation damage in DNA and RNA--repair mechanisms and medical significance. (2004, background): “coli has two genes for DNA repair methyltransferases, the inducibleada of the Ada regulon, andogt which is constitutively expressed [7,52].”
Genetic analyses from ancient DNA. (2004, background): “The most common form of such modification is the hydrolytic loss of amino groups from the bases adenine, cytosine, 5-methylcytosine, and guanine, resulting in hypoxanthine, uracil, thymine, and xanthine, respectively (31).”
Caenorhabditis elegans: An Emerging Model in Biomedical and Environmental Toxicology (2008, background): “Nucleotide excision repair is a critical pathway in the context of exposure to environmental toxins since it recognizes and repairs a wide variety of bulky, helix-distorting DNA lesions, including polycyclic aromatic hydrocarbon metabolites, mycotoxins such as aflatoxin B1, UV photoproducts, cisplat”
Genomic and Molecular Landscape of DNA Damage Repair Deficiency across The Cancer Genome Atlas (2018, unknown): “Homology-dependent recombination (HR), non-homologous end joining (NHEJ), the Fanconi anemia (FA) pathway, and translesion DNA synthesis (TLS) act alone or together to repair DNA strand breaks and complex events like interstrand crosslinks (Friedberg et al., 2004; Kass et al., 2016).”
Sub-lethal antibiotic treatment leads to multidrug resistance via radical-induced mutagenesis (2010, background): “Certain ROS, such as hydroxyl radicals, can directly damage DNA and lead to an accumulation of mutations (Demple and Harrison , 1994; Friedberg et al., 2006; Imlay et al., 1988).”
Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair (2010, background): “CPDs correspond to the formation of a four-member ring structure involving C5 and C6 of both neighboring bases whereas 6-4PPs are formed by a noncyclic bond between C6 (of the 5′-end) and C4 (of the 3′-end) of the involved pyrimidines via spontaneous rearrangement of the oxetane (when the 3′-end is ”
Nucleotide excision repair in eukaryotes. (2013, background): “The transcription and NER factor TFIIH is the next factor to join the NER complex and it is recruited by direct interaction with the XPCRAD23B protein (Evans et al. 1997a; Yokoi et al. 2000; Araujo et al. 2001; Volker et al. 2001; Riedl et al. 2003; Friedberg et al. 2005).”
A genome-wide view of the spectrum of spontaneous mutations in yeast (2008, background): “This biased pattern of mutation is consistent with observations on nucleotide instability: Spontaneous deamination of cytosine or 5-methylcytosine is a major source of C:G3 T:A transitions; and the conversion of guanine to 8-oxo-guanine (GO) is a major source of C:G3 A:T transversions (14, 15).”
DNA Replication Fidelity* (2004, background): “Genome stability also requires the ability to repair DNA damage that comes in many forms and is repaired by several different pathways (6), most of which require DNA synthesis to fill gaps created when lesions are excised.”