The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer.
By J. Smith, L. Tho, Naihan Xu, David A. Gillespie. Advances in Cancer Research, 2010
1,239 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/2f9311ac547f9b153d3ff9ffdc11c149fd2e988a
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Citations in the corpus
- DNA damage sensing by the ATM and ATR kinases. (2013, background): “Development of highly specific inhibitors of ATM, Chk1, and Chk2 has made promising progress (Smith et al. 2010).”
- Molecular mechanisms of cisplatin resistance (2012, neutral): “recombination (HR) (Smith et al., 2010).”
- Systems biology of cisplatin resistance: past, present and future (2014, background): “CDDP-elicited DNA adducts can engender double-strand breaks (DSBs), which are normally repaired along with DNA synthesis (or shortly after) via homologous recombination (HR).(136) Accordingly, HR-deficient neoplasms, such as those bearing loss-of-function mutations in the genes encoding breast cance”
- Role of hypoxia in cancer therapy by regulating the tumor microenvironment (2019, background): “For example, the E3 ubiquitin ligase Smurf1 determines cell apoptosis rates downstream of DNA damage–induced ATR–Chk1 signaling by promoting the death of transformed cells [107, 108].”
- Mechanisms of chemoresistance in cancer stem cells (2013, background): “This in turn impairs CDC25 family member activation of cyclin dependent kinases (CDKs) and G1/S and G2/M transitions [94].”