A correction has been issued for a research article published in Nature on January 14, 2026, concerning polyamine-dependent metabolic shielding and its influence on alternative splicing. The original publication contained an error in Figure 1g, where labels for "SAT1, SMARCA1, and ACTB" were incorrectly labeled as "24 h."
The correction, which addresses a labeling error within a figure, does not impact the overall conclusions of the study, according to the authors. The corrected figure is now available in both the HTML and PDF versions of the article on the Nature website. Alternative splicing, a fundamental process in molecular biology, allows a single gene to code for multiple proteins. This process is influenced by various factors, including cellular metabolism. Polyamines, organic compounds essential for cell growth and differentiation, play a role in this metabolic regulation. The research, conducted by scientists at the Center for Cooperative Research in Biosciences (CIC bioGUNE) in Derio, Spain, investigated how polyamines contribute to the shielding of metabolic processes that affect alternative splicing.
The research team, comprised of Amaia Zabala-Letona, Mikel Pujana-Vaquerizo, and colleagues, utilized metabolomics techniques to analyze the intricate relationship between polyamine metabolism and RNA splicing. Metabolomics, the large-scale study of small molecules within cells, provided a comprehensive view of the metabolic landscape. The initial error in Figure 1g involved mislabeling three right-hand labels reading 24 h, which should have read SAT1, SMARCA1 and ACTB. This error has been rectified in the current online version of the article.
The corrected data does not change the interpretation of the results, which suggest that polyamine metabolism is intricately linked to alternative splicing regulation. This finding could have implications for understanding various diseases, including cancer, where alternative splicing is often dysregulated. Researchers believe that a deeper understanding of these mechanisms could lead to the development of novel therapeutic strategies targeting metabolic pathways to modulate alternative splicing. The authors encourage readers to refer to the updated version of the article for accurate information.
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