Activation of a unique p53-dependent DNA damage response
Explore this paper's citation graph
Summary
The data indicate that unlike the DNA-damaging agents used here, RITA uniquely activates a p53-dependent DNA damage response, which may lead to a potential strategy for improving the therapeutic targeting of hypoxic tumor cells.
- Type
- letter
- Published
- 2009-05-15
- Cited by
- 15
- References
- 0
- Access
- Open access
- OpenAlex
- https://openalex.org/W2019081978
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:13089272
Keywords
DNA damage, Biology, DNA, Cell biology, Cell cycle
References
No references recorded for this paper.
Cited by
- RITA can induce cell death in p53-defective cells independently of p53 function via activation of JNK/SAPK and p38
- Small Molecules as Research Tools for Studying the Biology of the Tumour Suppressor p53
- Small-molecule inhibitors of the p53-MDM2 interaction.
- Modulation of p53's transcriptional function by small molecules
- Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA non-homologous end-joining
- Wild type p53 reactivation: From lab bench to clinic
- Awakening guardian angels: drugging the p53 pathway
- p53-based cancer therapy.
- Targeting tumour hypoxia to prevent cancer metastasis. From biology, biosensing and technology to drug development: the METOXIA consortium
- Pharmacological activation of a novel p53-dependent S-phase checkpoint involving CHK-1
- APE1-mediated DNA damage repair provides survival advantage for esophageal adenocarcinoma cells in response to acidic bile salts
- Novel phenylenediamine bridged mixed ligands dimetallic square planner Pt(II) complex inhibits MMPs expression via p53 and caspase-dependent signaling and suppress cancer metastasis and invasion.
- p53 in the Clinics
- Aloin promotes A549 cell apoptosis via the reactive oxygen species‑mitogen activated protein kinase signaling pathway and p53 phosphorylation.
- p53-Reactivating Molecules as Research Tools and Anticancer Drugs
Related papers
- Resisting Arrest: Recovery from Checkpoint Arrest Through Dephosphorylation of Chk1 by PP1
- Nek6 is involved in G2/M phase cell cycle arrest through DNA damage-induced phosphorylation
- Establishment of and recovery from damage checkpoint requires sequential interactions of Crb2 with protein kinases Rad3, Chk1, and Cdc2.
- The anaphase inhibitor of Saccharomyces cerevisiae Pds1p is a target of the DNA damage checkpoint pathway.
- Elevated Cyclin G2 Expression Intersects with DNA Damage Checkpoint Signaling and Is Required for a Potent G2/M Checkpoint Arrest Response to Doxorubicin*
- p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage.
- Cell-cycle checkpoint kinases: checking in on the cell cycle.
- The Schizosaccharomyces pombe S-phase checkpoint differentiates between different types of DNA damage.
- Novel checkpoint 1 inhibitors.