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RNA modifications are known to play a critical role in gene regulation and cellular processes. Specifically, N4-acetylcytidine (ac4C) modification has emerged as a significant marker involved in mRNA translation efficiency, stability, and various diseases. Accurate identification of ac4C modification sites is essential for unraveling its functional implications. However, currently available experimental methods suffer from drawbacks such as lengthy detection times, complexity, and high costs, resulting in low efficiency and accuracy in prediction. Although several bioinformatics methods have been proposed and have advanced the prediction of ac4C modification sites, there is still ample room for improvement. In this research, we propose a novel deep learning model, ERNIE-ac4C, which combines the ERNIE-RNA language model and a two-dimensional Convolutional Neural Network (CNN). ERNIE-ac4C utilizes the fusion of sequence features and attention map features to predict ac4C modification sites. ERNIE-ac4C surpasses other state-of-the-art deep learning methods, demonstrating superior accuracy and effectiveness. The availability of the code on GitHub (https://github.com/lrlbcxdd/ERNIEac4C.git) and our openness to feedback from the research community contribute to the model's accessibility and its potential for further advancements. Our study provides valuable insights into ac4C research and enhances our understanding of the functional consequences of RNA modifications.
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http://dx.doi.org/10.1016/j.jmb.2025.168978 | DOI Listing |
Methods
August 2025
School of Software, Shandong University, Jinan, China. Electronic address:
RNA N4-acetylcytidine (ac4C) modification plays a vital role in gene regulation and cellular function. Accurate identification of ac4C sites is essential for elucidating their biological significance. However, existing prediction methods struggle to capture complex sequence patterns, limiting their accuracy.
View Article and Find Full Text PDFFront Cell Dev Biol
August 2025
Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, Stem Cell and Cancer Center, The First Hospital of Jilin University, Changchun, China.
N4-acetylcytidine (ac4C) is an evolutionarily conserved RNA modification catalyzed by the acetyltransferase NAT10. It regulates RNA stability, translation, and post-transcriptional processes. Meanwhile, NAT10 functions as a dual-function enzyme exhibiting both protein acetyltransferase and RNA acetylase activities.
View Article and Find Full Text PDFInt J Biol Sci
August 2025
Department of General Surgery & Nanfang Gastrointestinal Cancer Institute (NGCI), Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P. R. China.
Tumor vascular normalization has emerged as a promising strategy to potentiate immune checkpoint blockade in solid tumors. Here, we unveil a previously unrecognized NAT10/XIST/YAP1/VEGFA signaling axis driving vascular abnormalization in gastric cancer (GC) and demonstrate its therapeutic potential in remodeling the tumor immune microenvironment. Through integrative analysis of acetylated RNA immunoprecipitation sequencing (acRIP-seq) and functional validation, we identified NAT10-mediated N4-acetylcytidine (ac4C) modification as a critical stabilizer of lncRNA XIST.
View Article and Find Full Text PDFPancreas
September 2025
State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital.
Objectives: To elucidate the role of N-acetyltransferase 10 (NAT10) in pancreatic cancer (PC) progression and its epigenetic mechanisms, particularly in relation to metastasis.
Methods: TCGA and GTEx databases were used to analyze the expression and roles of NAT10 in pancreatic cancer. We constructed stable cell lines with NAT10 knockdown in PC cell lines, AsPC-1 and KPC.
Genome Med
August 2025
Biotherapy Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.
Background: The epidemiological observational studies unveiled that aging is one of the risk factors for liver fibrosis, and the hepatic tissues in the elderly harbor more fibrotic lesions when compared to those in young people. Previous investigations found that TGFβ1 was elevated with aging and promoted liver fibrosis. However, the underlying mechanisms of aging and liver fibrosis remain largely unknown.
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