ArticleMolecular cell2008
Chk2 suppresses the oncogenic potential of DNA replication-associated DNA damage.
Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 67 citations in OpenAlex.
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- An introduction for the special issue on environmental health and genome integrity.Environmental and molecular mutagenesis · 2020Review
- A P53-Independent DNA Damage Response Suppresses Oncogenic Proliferation and Genome Instability.Cell reports · 2020Article
- Attenuated DNA damage responses and increased apoptosis characterize human hematopoietic stem cells exposed to irradiation.Scientific reports · 2018Article
- Betanodavirus B2 protein triggers apoptosis and necroptosis in lung cancer cells that suppresses autophagy.Oncotarget · 2017Article
- The Mre11-Nbs1 Interface Is Essential for Viability and Tumor Suppression.Cell reports · 2017Article
- Hydroxyurea Induces Cytokinesis Arrest in Cells Expressing a Mutated Sterol-14α-Demethylase in the Ergosterol Biosynthesis Pathway.Genetics · 2016Article
- Inner nuclear membrane protein Lem2 facilitates Rad3-mediated checkpoint signaling under replication stress induced by nucleotide depletion in fission yeast.Cellular signalling · 2016Article
- Article
- Defining ATM-Independent Functions of the Mre11 Complex with a Novel Mouse Model.Molecular cancer research : MCR · 2016Article
- EXO1 is critical for embryogenesis and the DNA damage response in mice with a hypomorphic Nbs1 allele.Nucleic acids research · 2015Article
- Replication stress and cancer.Nature reviews. Cancer · 2015Review
- A PREVIOUSLY UNKNOWN UNIQUE CHALLENGE FOR INHIBITORS OF SYK ATP-BINDING SITE: ROLE OF SYK AS A CELL CYCLE CHECKPOINT REGULATOR.EBioMedicine · 2014Article
- Role of DNA damage response pathways in preventing carcinogenesis caused by intrinsic replication stress.Oncogene · 2014Article
- USP28 is recruited to sites of DNA damage by the tandem BRCT domains of 53BP1 but plays a minor role in double-strand break metabolism.Molecular and cellular biology · 2014Article
- Ataxia-telangiectasia: future prospects.The application of clinical genetics · 2014Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The Mre11 complex (Mre11, Rad50, and Nbs1) and Chk2 have been implicated in the DNA-damage response, an inducible process required for the suppression of malignancy. The Mre11 complex is predominantly required for repair and checkpoint activation in S phase, whereas Chk2 governs apoptosis. We examined the relationship between the Mre11 complex and Chk2 in the DNA-damage response via the establishment of Nbs1(DeltaB/DeltaB) Chk2(-/-) and Mre11(ATLD1/ATLD1) Chk2(-/-) mice. Chk2 deficiency did not modify the checkpoint defects or chromosomal instability of Mre11 complex mutants; however, the double-mutant mice exhibited synergistic defects in DNA-damage-induced p53 regulation and apoptosis. Nbs1(DeltaB/DeltaB) Chk2(-/-) and Mre11(ATLD1/ATLD1) Chk2(-/-) mice were also predisposed to tumors. In contrast, DNA-PKcs-deficient mice, in which G1-specific chromosome breaks are present, did not exhibit synergy with Chk2(-/-) mutants. These data suggest that Chk2 suppresses the oncogenic potential of DNA damage arising during S and G2 phases of the cell cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.