ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
By L. Toledo, M. Altmeyer, M. Rask, C. Lukas, D. Larsen, L. Povlsen, Simon Bekker-Jensen, Niels Mailand, J. Bartek, J. Lukas. Cell, 2013
885 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/eefc765c11d4d15c208581c19488ab827cad99fa
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Stephen P. Jackson
- Andrew N. Blackford
- Morgane Macheret
- T. Halazonetis
- J. Bartek
- Yosef Shiloh
- Y. Fouad
- C. Aanei
Citations in the corpus
- DNA replication stress as a hallmark of cancer. (2015, positive): “In one study, U2OS cells were treated with the Wee1 inhibitor MK-1775 to enhance origin firing and, in parallel, fork progression was challenged with hydroxyurea (98).”
- ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, positive): “This is important to avoid exhaustion of replication and repair factor pools, particularly RPA (Toledo et al., 2013).”