Repair and genetic consequences of endogenous DNA base damage in mammalian cells.
By D. Barnes, Tomas Lindahl. Annual Review of Genetics, 2004
751 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/6943b505b17e28be909e55a31d87c596c07d3a00
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- D. Hanahan
- R. Weinberg
- Carol Prives
- A. Gorman
- Simone Fulda
- Afshin Samali
- Lisa M. Coussens
- Raghu Kalluri
In Molecular Biology
- D. Hanahan
- R. Weinberg
- William A. Freed-Pastor
- Carol Prives
- Rajeshwar Prasad Sinha
- A. Gorman
- Simone Fulda
- Afshin Samali
In Pathology and Forensic Medicine
Citations in the corpus
- Mechanism and regulation of class switch recombination. (2008, background): “Enzyme assays using abasic site-containing oligonucleotide substrates showed that purified recombinant human APE2 has weaker AP endonuclease activity than APE1 (65, 72, 73).”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Base damage can be repaired either by enzyme-catalyzed reversal or alternatively via excision repair [183].”
- Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair (2010, background): “As a result of multiple interactions with a number of repair proteins XRCC1 plays a crucial role in the coordination of BER and SSB repair [189].”
- Mutant p53: one name, many proteins. (2012, background): “This is likely due to the fact that the cytosine in this dinucleotide is frequently methylated; spontaneous deamination can occur, changing the cytosine to uracil, and the resulting U:G mispair can give rise to a C:G-toT:A transition (Barnes and Lindahl 2004).”
- Hallmarks of cancer: the next generation. (2011, positive): “Mutant copies of many of these care-taker genes have been introduced into the mouse germline and result, predictably, in increased cancer incidence, supporting their potential involvement in human cancer development ( Barnes and Lindahl, 2004).”
- Role of oxidative stress and DNA damage in human carcinogenesis. (2011, background): “These transient apurinic sites though cannot be considered per se as oxidatively generateddamage toDNAbut theyhavebeen shown to accumulate in cells and tissue at significant numbers that can reach or exceed ∼10,000/cell/day [30–33].”
- Base-excision repair of oxidative DNA damage (2007, background): “This enzyme catalyses the removal of uracil from DNA, the first step of the base-excision repair (BER) pathwa”