Nucleic Acids Research

Nucleic Acids Research

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Nucleic Acids Research (NAR), from Oxford University Press, publishes the results of leading-edge research into physical, chemical, biochemical and biological aspects of nucleic acids and proteins involved in nucleic acid metabolism and/or interactions

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Hello Everyone! 👋 Nucleic Acids Research is excited to be on Bluesky! Please follow us for the latest #Research, #Breakthrough articles, journal issues and more. Also, please consider adding us to your starter packs!

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16. #CDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombination - Brown et al. doi.org/10.1093/narc.... Addresses the session's cell-cycle/replication repair interface by connecting cyclin-CDK2 activity to HR repair of collapsed forks. 17/18

doi.orgCDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombinationAbstract. CCNE1 amplification is a common alteration in high-grade serous ovarian cancer and occurs in 15–20% of these tumors. These amplifications are mut
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17. Dual inhibition of DNA-PK and DNA polymerase theta overcomes radiation resistance induced by p53 deficiency - Kumar et al. doi.org/10.1093/narc.... Dual DNA-PK/POLθ inhibition restores radiation sensitivity in p53-deficient models. 18/18

doi.orgDual inhibition of DNA-PK and DNA polymerase theta overcomes radiation resistance induced by p53 deficiencyAbstract. TP53 deficiency in cancer is associated with poor patient outcomes and resistance to DNA damaging therapies. However, the mechanisms underlying t
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14. Targeting DNA repair mechanisms in cancer therapy: the role of #smallmolecule #DNArepair inhibitors - Jeong et al. doi.org/10.1093/narc... “Editor’s Choice” review article detailing the current pipeline of repair inhibitors, synthetic lethality, biomarkers, and their combinations. 15/18

doi.orgTargeting DNA repair mechanisms in cancer therapy: the role of small molecule DNA repair inhibitorsAbstract. Genomic instability and the accumulation of DNA damage are hallmarks of cancer, often resulting from defects in DNA repair pathways. While normal
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15. Harnessing transcriptional regulation of alternative end-joining to predict cancer treatment - Espín et al. doi.org/10.1093/narc... Links #hypoxia/HIF1α and #MYC to #PARP1/POLQ expression and alternative end joining, with combination-treatment effects in cancer cells. 16/18

doi.orgHarnessing transcriptional regulation of alternative end-joining to predict cancer treatmentAbstract. Alternative end-joining (alt-EJ) is an error-prone DNA repair pathway that cancer cells deficient in homologous recombination rely on, making the
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12. Defining the mutation signatures of #DNApolymeraseθ in cancer genomes - Hwang et al. doi.org/10.1093/narc.... Links BRCA loss to dependence on polymerase theta–mediated end joining and the resulting mutational landscape. 13/18

doi.orgDefining the mutation signatures of DNA polymerase θ in cancer genomesAbstract. DNA polymerase theta (POLQ)-mediated end joining (TMEJ) is a distinct pathway for mediating DNA double-strand break (DSB) repair. TMEJ is require
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13. Regulation and #pharmacological targeting of #RAD51 in cancer - Grundy et al. doi.org/10.1093/narc.... Review article on RAD51, the central recombinase regulated by BRCA2, PALB2 and RAD51 paralogs, linking HR control to #cancerprevention and #therapeuticresistance. 14/18

doi.orgRegulation and pharmacological targeting of RAD51 in cancerAbstract. Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too m
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10. #Homologous recombination, cancer and the ‘RAD51 paradox’ - Matos-Rodrigues et al. doi.org/10.1093/narc.... BRCA1, BRCA2, PALB2 and RAD51-associated factors placed within HR, replication-fork maintenance, cancer susceptibility, and the consequences of dysregulated recombination. 11/18

doi.orgHomologous recombination, cancer and the ‘RAD51 paradox’Abstract. Genetic instability is a hallmark of cancer cells. Homologous recombination (HR) plays key roles in genome stability and variability due to its r
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11. Characterization of a RAD51C-silenced high-grade serous #ovarian cancer model during development of PARP inhibitor resistance - Hurley et al. doi.org/10.1093/narc.... A non-mutational route to PARP inhibitor resistance through loss of RAD51C #promotermethylation and restored expression. 12/18

doi.orgCharacterization of a RAD51C-silenced high-grade serous ovarian cancer model during development of PARP inhibitor resistanceAbstract. Acquired PARP inhibitor (PARPi) resistance in BRCA1- or BRCA2-mutant ovarian cancer often results from secondary mutations that restore expressio
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9. High-level tumour #methylation of #BRCA1 and #RAD51C is required for #homologousrecombination deficiency in solid cancers - Xu et al doi.org/10.1093/narc.... Extends BRCA-network deficiency beyond sequence mutations to #epigeneticsilencing. 10/18

doi.orgHigh-level tumour methylation of BRCA1 and RAD51C is required for homologous recombination deficiency in solid cancersAbstract. In ovarian and breast cancer, promoter methylation of BRCA1 or RAD51C is a promising biomarker for PARP inhibitor response, as high levels lead t
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6. #XRCC1 promotes replication restart, nascent fork degradation, and mutagenic DNA repair... Eckelmann et al. doi.org/10.1093/narc.... How does an alternative repair scaffold support BRCA2-deficient cells through altered fork processing and mutagenic repair? 7/18

doi.orgXRCC1 promotes replication restart, nascent fork degradation and mutagenic DNA repair in BRCA2-deficient cellsAbstract. Homologous recombination/end joining (HR/HEJ)-deficient cancers with BRCA mutations utilize alternative DNA double-strand break repair pathways,
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7. Therapeutic disruption of RAD52–ssDNA complexation via novel drug-like inhibitors - Bhat et al. doi.org/10.1093/narc.... A concrete example of emerging therapeutics: identifies and optimizes RAD52 inhibitors with selective toxicity in BRCA-mutant cells. 8/18

doi.orgTherapeutic disruption of RAD52–ssDNA complexation via novel drug-like inhibitorsAbstract. RAD52 protein is a coveted target for anticancer drug discovery. Similar to poly-ADP-ribose polymerase (PARP) inhibitors, pharmacological inhibit
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4. The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells - Hale et al. doi.org/10.1093/narc.... How #PARP14 engages nascent DNA and recruits MRE11 to degrade reversed forks in BRCA2-deficient cells. 5/18

doi.orgThe RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cellsAbstract. Degradation of reversed replication forks by nucleases has emerged as a major mechanism of chemosensitivity in BRCA-deficient cells. We previousl
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5. Advancing inducible gene-inactivation systems to explore synthetic lethality - Sánta et al. doi.org/10.1093/narc.... Combined BRCA1 and RAD18 loss compromises fork restart and post-replicative gap filling, producing ssDNA gaps and replication catastrophe. 6/18

doi.orgAdvancing inducible gene-inactivation systems to explore synthetic lethalityAbstract. Synthetic lethality offers opportunities to identify therapeutic targets for cancer research, facilitating the development of targeted tumour the
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2. RAD51C breast cancer-identified variants with attenuated homologous recombination function... Ganesan et al. doi.org/10.1093/narc... #RAD51C variants retain partial #HR yet disrupt replication and accumulate gaps; a subset sensitizes cells to combined #PARP1 and #ATR inhibition. 3/18

doi.orgRAD51C breast cancer-identified variants with attenuated homologous recombination function exhibit sensitivity to combined PARP1 and ATR inhibitionAbstract. The tumor suppressor RAD51C is essential for DNA double-strand break repair through the homologous recombination (HR) pathway. RAD51C loss is lin
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3. Mechanisms of PARP1 inhibitor resistance and their implications for cancer treatment - Jackson & Moldovan. doi.org/10.1093/narc... #HRrestoration, #replication-fork stabilization, #ssDNA-gap suppression, and strategies to overcome PARP inhibitor resistance. 4/18

doi.orgMechanisms of PARP1 inhibitor resistance and their implications for cancer treatmentAbstract. The discovery of synthetic lethality as a result of the combined loss of PARP1 and BRCA has revolutionized the treatment of DNA repair-deficient
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1.STN1 upregulation promotes #PARPiresistance in BRCA2-deficient cancer cells via replication fork protection... Laghari et al. #BRCA2 loss, #RAD51 loading, #MRE11 exclusion, #forkprotection, and suppression of ssDNA gaps linked to #PARPi resistance doi.org/10.1093/narc... 2/18

doi.orgSTN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formationAbstract. PARPi are effective therapy for BRCA1/2 mutant cancers, yet recurrent PARPi resistance frequently develops. The underlying mechanism of PARPi res
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⭐ Celebrating the Launch of the Human Genome Project (HPG) 🧬36 years ago today, scientists launched one of biology’s most ambitious experiments: reading the ~3 billion bases of the human genome. On Oct. 1, 1990, HPG began with a seemingly impossible question: Could we sequence the human genome? 1/5

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📖 But “HGP vs. Celera” doesn’t tell the whole story. Celera generated its own shotgun data, but its 2001 Science analysis also incorporated publicly available HGP sequence data. Competition, shared data, and computation all played a role. 4/5

Nucleic Acids Research
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The Human Genome Project didn’t end genomics—it opened the door. Its sequence helped fuel #precisionmedicine, #cancergenomics, #genetherapy and #genomeediting. And it revealed a deeper question: 🧬 How is the genome regulated? Enter the world of #Epigenetics. #HumanGenomeProject #HGP #Genomics

Nucleic Acids Research
@narjournal.bsky.social

⭐ Celebrating the Launch of the Human Genome Project (HPG) 🧬36 years ago today, scientists launched one of biology’s most ambitious experiments: reading the ~3 billion bases of the human genome. On Oct. 1, 1990, HPG began with a seemingly impossible question: Could we sequence the human genome? 1/5

Nucleic Acids Research
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🔬The challenge demanded mapping, new technologies, automation and computation—and two competing strategies: 🌍 Public HGP: map → sequence → assemble 💻 Celera: sequence → computationally assemble Different approaches. One extraordinary challenge. 2/5

Nucleic Acids Research
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⚡The scale was staggering: 🌍 Public HGP: ~600 sequencers across 20 institutions in 6 countries ⚡ Celera: ~300 sequencers in one facility. By 2000, competing drafts had emerged. In 2001, landmark papers appeared in Nature and Science. 3/5

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Congratulations to the authors on their #NARCANCER publication! 🎉 Deleterious #SMC5/6 variants may predict higher #tumormutationalburden and better responses to #immunotherapy, highlighting their potential as #biomarkers for #precisioncancertherapy.

Bill Dynan - NAR Cancer Editor@nar-cancer-editor.bsky.social

Can SMC5/6 status help guide precision cancer therapy? A new NAR Cancer study links deleterious SMC5/6 variants to tumor mutational burden and immunotherapy responses, driven via POLE dysfunction and mismatch repair deficiency.https://academic.oup.com/narcancer/article/8/2/zcag012/8688771

academic.oup.comDisruption of the structural maintenance of chromosomes 5/6 complex enables tumor mutagenesisAbstract. The structural maintenance of chromosomes (SMC) 5/6 complex is conserved and essential for mammalian development. SMC5/6 germline variants in cel
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📣The 24th annual NAR Web Server Issue is now online! 📣Explore 47 new web servers spanning a range of scientific and medical applications. Congratulations and thanks to all authors, editors and reviewers for your contributions!🧬 #NARWebServer #MolecularBiology #OpenAccessIssue

Nucleic Acids Research
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📣 Applications are open for the next NAR Early Career Investigator (ECI) Advisory Board cohort! Work with Executive Editors, help shape journal strategy, and gain insight into peer review during a 2-year term. Apply by 1 Nov 2026: lnkd.in/g233ZCAf #ECR #NAR #AcademicPublishing #MolecularBiology

Nucleic Acids Research
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Big congratulations to the authors! 🎉🦠 Using RNA-seq, this study uncovers overlooked viral RNA species and supports a premature termination model for astrovirus subgenomic RNA synthesis, resolving a long-standing replication mystery. 🔬✨ #NARMolecularMedicine #Virology @universitypress.cambridge.org

Valeria Lulla@valerialulla.bsky.social

🚨 New paper from the lab! 🚀 We explore “The dynamics and strategy of RNA replication in astroviruses”, now out in NAR Molecular Medicine. Many thanks to all co-authors and congratulations to David Noyvert on his first first-author paper🎉 doi.org/10.1093/narm...

doi.orgThe dynamics and strategy of RNA replication in astrovirusesAbstract. Astroviruses are positive-sense single-stranded RNA viruses that cause significant disease across avian and mammalian hosts, yet their replicatio

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Bill Dynan - NAR Cancer Editor
@nar-cancer-editor.bsky.social

Few cancer driver mutations have been identified in promoters, maybe for technical reasons. New assay targets >3,000 promoters — hits in CDK4, SMAD3, and GATA3 in breast cancer provide promising leads for functional follow-up. academic.oup.com/narcancer/ar... #CancerGenomics #NonCoding #Promoters

academic.oup.comSensitive detection of somatic mutations in GC-rich cancer gene promotersAbstract. Somatic mutations in protein-coding genes and noncoding regulatory regions are the major drivers of cancer. Only a relatively small number of som