ArticleMolecular and cellular biology2009
Rad50 is dispensable for the maintenance and viability of postmitotic tissues.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Bone Marrow Failure and Immunodeficiency Associated with Human RAD50 Variants.Journal of clinical immunology · 2023Article
- ISG15 conjugation to proteins on nascent DNA mitigates DNA replication stress.Nature communications · 2022Article
- The Essential DNA Damage Response Complex MRN Is Dispensable for the Survival and Function of Purkinje Neurons.Frontiers in aging neuroscience · 2021Article
- A Disease-Causing Single Amino Acid Deletion in the Coiled-Coil Domain of RAD50 Impairs MRE11 Complex Functions in Yeast and Humans.Cell reports · 2020Article
- NBS1 interacts with Notch signaling in neuronal homeostasis.Nucleic acids research · 2020Article
- Review
- Nbn-Mre11 interaction is required for tumor suppression and genomic integrity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- ATM in breast and brain tumors: a comprehensive review.Cancer biology & medicine · 2018Article
- TET3-mediated DNA oxidation promotes ATR-dependent DNA damage response.EMBO reports · 2017Article
- The Mre11-Nbs1 Interface Is Essential for Viability and Tumor Suppression.Cell reports · 2017Article
- Synthetic lethality in ATM-deficient RAD50-mutant tumors underlies outlier response to cancer therapy.Cancer discovery · 2014Article
- Rad50-CARD9 interactions link cytosolic DNA sensing to IL-1β production.Nature immunology · 2014Article
- The Rad50 hook domain regulates DNA damage signaling and tumorigenesis.Genes & development · 2014Article
- Article
- Hypersensitive site 6 of the Th2 locus control region is essential for Th2 cytokine expression.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Terminal differentiation of cardiac and skeletal myocytes induces permissivity to AAV transduction by relieving inhibition imposed by DNA damage response proteins.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- A polyglutamine expansion disease protein sequesters PTIP to attenuate DNA repair and increase genomic instability.Human molecular genetics · 2012Article
- Chemical genetics reveals a specific requirement for Cdk2 activity in the DNA damage response and identifies Nbs1 as a Cdk2 substrate in human cells.PLoS genetics · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The majority of spontaneous chromosome breakage occurs during the process of DNA replication. Homologous recombination is the primary mechanism of repair of such damage, which probably accounts for the fact that it is essential for genome integrity and viability in mammalian cells. The Mre11 complex plays diverse roles in the maintenance of genomic integrity, influencing homologous recombination, checkpoint activation, and telomere maintenance. The complex is essential for cellular viability, but given its myriad influences on genomic integrity, the mechanistic basis for the nonviability of Mre11 complex-deficient cells has not been defined. In this study we generated mice carrying a conditional allele of Rad50 and examined the effects of Rad50 deficiency in proliferative and nonproliferative settings. Depletion of Rad50 in cultured cells caused extensive DNA damage and death within 3 to 5 days of Rad50 deletion. This was not associated with gross telomere dysfunction, suggesting that the telomeric functions of the Mre11 complex are not required for viability. Rad50 was also dispensable for the viability of quiescent liver and postmitotic Purkinje cells of the cerebellum. These findings support the idea that the essential functions of the Mre11 complex are associated with DNA replication and further suggest that homologous recombination is not essential in nondividing cells.
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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.