ReviewCancers2020
Physiological and Pathological Roles of RAD52 at DNA Replication Forks.
Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 25 citations in OpenAlex.
- CHK2 regulates MUS81-dependent DSBs in response to replication stress and BRCA2 deficiency.Nucleic acids research · 2026Article
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- Article
- RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024Article
- Deficiency in homologous recombination is associated with changes in cell cycling and morphology in Saccharomyces cerevisiae.Experimental cell research · 2023Article
- Article
- Roles of homologous recombination in response to ionizing radiation-induced DNA damage.International journal of radiation biology · 2023Review
- A moving target for drug discovery: Structure activity relationship and many genome (de)stabilizing functions of the RAD52 protein.DNA repair · 2022Review
- KMT2C-deficient tumors have elevated APOBEC mutagenesis and genomic instability in multiple cancers.NAR cancer · 2022Article
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- Review
- KERA: analysis tool for multi-process, multi-state single-molecule data.Nucleic acids research · 2021Article
- Identification of a novel heterozygous germline RAD52 missense mutation in a patient with gallbladder carcinoma: A case report.Medicine · 2021Article
- Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021Review
- The function of RAD52 N-terminal domain is essential for viability of BRCA-deficient cells.Nucleic acids research · 2020Article
- RNA: a double-edged sword in genome maintenance.Nature reviews. Genetics · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Understanding basic molecular mechanisms underlying the biology of cancer cells is of outmost importance for identification of novel therapeutic targets and biomarkers for patient stratification and better therapy selection. One of these mechanisms, the response to replication stress, fuels cancer genomic instability. It is also an Achille's heel of cancer. Thus, identification of pathways used by the cancer cells to respond to replication-stress may assist in the identification of new biomarkers and discovery of new therapeutic targets. Alternative mechanisms that act at perturbed DNA replication forks and involve fork degradation by nucleases emerged as crucial for sensitivity of cancer cells to chemotherapeutics agents inducing replication stress. Despite its important role in homologous recombination and recombinational repair of DNA double strand breaks in lower eukaryotes, RAD52 protein has been considered dispensable in human cells and the full range of its cellular functions remained unclear. Very recently, however, human RAD52 emerged as an important player in multiple aspects of replication fork metabolism under physiological and pathological conditions. In this review, we describe recent advances on RAD52's key functions at stalled or collapsed DNA replication forks, in particular, the unexpected role of RAD52 as a gatekeeper, which prevents unscheduled processing of DNA. Last, we will discuss how these functions can be exploited using specific inhibitors in targeted therapy or for an informed therapy selection.
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What OpenQuestion holds
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.