ArticleCell reports2015
RECQL5 Suppresses Oncogenic JAK2-Induced Replication Stress and Genomic Instability.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Retrograde rearrangement of mitochondria correlates with nuclear deformation and genotoxic damage.iScience · 2025Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Calreticulin and JAK2V617F driver mutations induce distinct mitotic defects in myeloproliferative neoplasms.Scientific reports · 2024Article
- Review
- Recurrent germline variant in ATM associated with familial myeloproliferative neoplasms.Leukemia · 2023Article
- Insights into the Potential Mechanisms of JAK2V617F Somatic Mutation Contributing Distinct Phenotypes in Myeloproliferative Neoplasms.International journal of molecular sciences · 2022Review
- Genetic Factors Associated with Prostate Cancer Conversion from Active Surveillance to Treatment.HGG advances · 2022Article
- PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2Cancer discovery · 2020Article
- Review
- Article
- RECQL5 at theFrontiers in cell and developmental biology · 2020Review
- Broad regulation of gene isoform expression by Wnt signaling in cancer.RNA (New York, N.Y.) · 2019Article
- RECQL5 plays an essential role in maintaining genome stability and viability of triple-negative breast cancer cells.Cancer medicine · 2019Article
- Article
- Increased levels of RECQ5 shift DNA repair from canonical to alternative pathways.Nucleic acids research · 2018Article
- Lnk/Sh2b3 deficiency restores hematopoietic stem cell function and genome integrity in Fancd2 deficient Fanconi anemia.Nature communications · 2018Article
- Mechanisms for stalled replication fork stabilization: new targets for synthetic lethality strategies in cancer treatments.EMBO reports · 2018Review
- Molecular-genetic profiling and high-throughputOncotarget · 2017Article
- Insights into the RecQ helicase mechanism revealed by the structure of the helicase domain of human RECQL5.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
Abstract
JAK2V617F is the most common oncogenic lesion in patients with myeloproliferative neoplasms (MPNs). Despite the ability of JAK2V617F to instigate DNA damage in vitro, MPNs are nevertheless characterized by genomic stability. In this study, we address this paradox by identifying the DNA helicase RECQL5 as a suppressor of genomic instability in MPNs. We report increased RECQL5 expression in JAK2V617F-expressing cells and demonstrate that RECQL5 is required to counteract JAK2V617F-induced replication stress. Moreover, RECQL5 depletion sensitizes JAK2V617F mutant cells to hydroxyurea (HU), a pharmacological inducer of replication stress and the most common treatment for MPNs. Using single-fiber chromosome combing, we show that RECQL5 depletion in JAK2V617F mutant cells impairs replication dynamics following HU treatment, resulting in increased double-stranded breaks and apoptosis. Cumulatively, these findings identify RECQL5 as a critical regulator of genome stability in MPNs and demonstrate that replication stress-associated cytotoxicity can be amplified specifically in JAK2V617F mutant cells through RECQL5-targeted synthetic lethality.
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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.