ArticleHaematologica2022
Ddx41 inhibition of DNA damage signaling permits erythroid progenitor expansion in zebrafish.
Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Clinicopathological and prognostic significance of DDX41 mutation in myeloid neoplasms: a systematic review and meta-analysis.Annals of hematology · 2025Pooled it
- [Germline DDX41 mutations and myelodysplastic neoplasms].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Germline DDX41 mutations in myeloid neoplasms: a comprehensive review.The Korean journal of internal medicine · 2026Review
- Leveraging paired germline and somatic analysis to improve the classification of DDX41 variants.British journal of haematology · 2026Article
- BMP-Smad1/9 signaling plays a critical role in regulating zebrafish PGC proliferation.Nature communications · 2026Article
- MDS/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops.Nucleic acids research · 2026Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- Prpf4 sequentially regulates the expansion and maturation of erythrocyte through distinct mechanisms.Cell death discovery · 2025Article
- Overall cancer risk in people with deleterious germlineHaematologica · 2025Article
- DDX41 resolves G-quadruplexes to maintain erythroid genome integrity and prevent cGAS-mediated cell death.Nature communications · 2025Article
- Genotype-integrated single-cell transcriptome analysis reveals the role of DDX41 pR525H in a patient with myelodysplastic neoplasms.Scientific reports · 2025Article
- Germline DDX41 mutations in myeloid neoplasms: the current clinical and molecular understanding.Current opinion in hematology · 2025Review
- Post-transcriptional regulation of DEAD-box RNA helicases in hematopoietic malignancies.Genes & diseases · 2024Review
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- Article
- Pathogenic GATA2 genetic variants utilize an obligate enhancer mechanism to distort a multilineage differentiation program.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Nucleic acid-induced inflammation on hematopoietic stem cells.Experimental hematology · 2024Article
- Multifunctional role of DEAD-box helicase 41 in innate immunity, hematopoiesis and disease.Frontiers in immunology · 2024Review
- Article
- Unraveling DNA Repair Processes In Vivo: Insights from Zebrafish Studies.International journal of molecular sciences · 2023Review
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 1 institution in 1 country.
Funding
Abstract
DEAD-box Helicase 41 (DDX41) is a recently identified factor mutated in hematologic malignancies whose function in hematopoiesis is unknown. Using an in vivo model of Ddx41 deficiency, we unveiled a critical role for this helicase in regulating erythropoiesis. We demonstrated that loss of ddx41 leads to anemia caused by diminished proliferation and defective differentiation of erythroid progenitors. Mis-expression and alternative splicing of cell cycle genes is rampant in ddx41 mutant erythroid progenitors. We delineated that the DNA damage response is activated in mutant cells resulting in an Ataxiatelangiectasia mutated (ATM) and Ataxia-telangiectasia and Rad3-related (ATR)-triggered cell cycle arrest. Inhibition of these kinases partially suppressed ddx41 mutant anemia. These findings establish a critical function for Ddx41 in promoting healthy erythropoiesis via protection from genomic stress and delineate a mechanistic framework to explore a role for ATM and ATR signaling in DDX41-mutant hematopoietic pathologies.
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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.