Error-prone repair DNA polymerases in prokaryotes and eukaryotes.
By Myron F. Goodman. Annual Review of Biochemistry, 2002
729 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/2e41144b08ed6b467d246d84b1566933e442ffc8
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Citations in the corpus
- Repair of DNA Damage Induced by Solar UV (2004, background): “…they will proceed into a secondary ‘damage tolerance’ phase in which stalled DNA polymerases will be rolled back or removed from sites of damage, and a second set of less fastidious polymerases upregulated to perform ‘dimer bypass,’ the polymerization of DNA past a damaged site (Goodman 2002).”
- The role of specialized DNA polymerases in mutagenesis in Pseudomonas putida (2009, background): “14 for specialized DNA polymerases is enhanced by the induction of expression of these particular DNA polymerases as a response to DNA damage known as SOS-response (Hanaoka, 2001; Goodman, 2002).”
- Processive AID-catalysed cytosine deamination on single-stranded DNA simulates somatic hypermutation (2003, methodology): “Absent from our analysis are specific roles for error-prone polymerase”
- Proliferating cell nuclear antigen (PCNA): a dancer with many partners (2003, background): “An alternative pathway for DNA damage tolerance in eukaryotic cells is translesion synthesis (TLS), which relies on specialised polymerases able to carry on DNA synthesis on a damaged template (Goodman, 2002; Hubscher et al., 2002).”
- Loss of DNA Polymerase ζ Causes Chromosomal Instability in Mammalian Cells (2006, background): “For the Rev3L null cells, only one aberration identified in the first series [der(2)t(1;2)] was found in the second group, indicating that the chromosomal instability is a continuous process occurring cell by cell and dispersed throughout the mouse genome.”
- DNA damage and repair (2003, background): “One such damage-tolerance mechanism, called translesion DNA synthesis, involves the replication machinery bypassing sites of base damage, allowing normal DNA replication and gene expression to proceed downstream of the (unrepaired) damag”
- The role of DNA mismatch repair and oxidative DNA damage defense systems in avoidance of stationary phase mutations in Pseudomonas putida (2007, background): “5) 3 69 47 (68) 4 (6) 4 (6) 0 2 (3) 12 (17) 4 62 30 (48) 10 (16) 2 (3) 5 (8) 3 (5) 12 (20) 5 70 30 (43) 9 (13) 3 (4) 6 (9) 0 22 (31) 6 60 18 (30) 12 (20) 0 13 (22) 1 (2) 16 (26) 7 61 16 (26) 11 (18) 0 12 (20) 5 (8) 17 (28)”