ArticleNucleic acids research2026
DDX24 modulates angiogenesis by promoting CCR4-NOT complex-dependent mRNA decay.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
DEAD-box (DDX) RNA helicases play critical roles in gene regulation by interacting with RNAs and influencing RNA fate and function. Our previous study associated DDX24 dysfunction with vascular development, but its precise role in RNA metabolism in the context of angiogenesis remains unclear. Here, we identified DDX24-bound messenger RNAs (mRNAs) in endothelial cells using infrared cross-linking immunoprecipitation sequencing. We found that DDX24 modulates endothelial cell functions by directly binding to and regulating specific mRNA targets that are crucial for vascular development and angiogenesis, such as CLEC14A and ERG. Mechanistically, DDX24 promotes the decay of these mRNA targets in a CCR4-NOT deadenylase complex-dependent manner. These results establish a link between DDX24-dependent regulation of mRNA stability and endothelial cell function, providing novel therapeutic targets for angiogenesis-related diseases.
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