Homologous recombination in DNA repair and DNA damage tolerance
By Xuan Li, Wolf-Dietrich Heyer. Cell Research, 2008
1,175 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/6a68b8e450c67b17aa5e641426a23a692285f978
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
In Molecular Biology
- Thomas Helleday
- J. Smith
- Wolf-Dietrich Heyer
- Jie Liu
- Naihan Xu
- L. Tho
- David A. Gillespie
- Kirk T. Ehmsen
In Oncology
Citations in the corpus
- The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer. (2010, background): “…since when encountered by replicative polymerases they lead to replication fork collapse and formation of DSBs. HRR is thought to be the main mechanism through which such DSBs can be repaired and replication restarted, enabling HRR proficient cells to tolerate PARP inhibition (Li and Heyer, 2008).”
- Regulation of homologous recombination in eukaryotes (2010, background): “Recombination is required for the repair or tolerance of DNA damage and the recovery of stalled or broken replication forks (95).”
- Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair (2010, background): “RAD51, the eukaryotic RecA homolog, is an essential HR factor that catalyzes homology search and strand exchange (Baumann et al., 1996; Li and Heyer, 2008).”