生物学最新文献

{"title":"STED/AFM as a tool to investigate mechanical and adhesive properties of migrating keratinocytes.","authors":"Mariya Y Radeva, Jens Waschke, Michael Fuchs","doi":"10.1080/19336918.2026.2657675","DOIUrl":"10.1080/19336918.2026.2657675","url":null,"abstract":"<p><p>E-cadherin is a key component of adherens junctions which maintains epithelial integrity. In keratinocytes, wound healing requires dynamic modulation of adhesion and cytoskeletal organization. Using a wound healing assay combined with stimulated emission depletion/atomic force microscopy (STED/AFM), we analysed E-cadherin binding during murine keratinocyte migration. Wound closure occurred within 6 h and was accompanied by E-cadherin accumulation at the leading edge. Transient expression of E-Cadherin-SNAP enabled investigation of E-cadherin interactions. Inhibition of actin polymerization abolished E-cadherin binding and reduced cellular stiffness. Imaging of SiR-actin-labeled cells enabled simultaneous visualization of migration and measurement of binding and mechanical properties. E-cadherin retained functional binding properties during migration. These findings establish STED/AFM as a powerful method to investigate single-molecule binding properties in migrating cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"20 1","pages":"2657675"},"PeriodicalIF":4.3,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13089918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The RNA exosome: mechanisms of RNA surveillance, regulation, and disease.","authors":"Priyanka Upadhyai, Neha Quadri, Divya Chandran","doi":"10.1080/15476286.2026.2685379","DOIUrl":"10.1080/15476286.2026.2685379","url":null,"abstract":"<p><p>The RNA exosome is a conserved multi-subunit ribonuclease complex with pivotal roles in RNA biogenesis, surveillance, and processing. It comprises a nine-subunit scaffold that associates with distinct ribonucleases in a cell compartment-specific manner, contributing to the processing and turnover of a broad spectrum of nuclear and cytoplasmic transcripts, including pervasively transcribed and short-lived RNAs, precursors, and abortive and aberrant transcripts. In this review, we examine how the RNA exosome engages a wide spectrum of RNAs via differential adaptor usage and intrinsic substrate features, such as transcript length and 3' end structure. This also modulates the entry routes of the recruited transcripts. We highlight conserved principles and major differences between yeast and metazoans. We assimilate emerging evidence that suggests that the RNA exosome localization and activity are dynamically regulated in response to cellular context and external stimuli. Finally, drawing on findings from studies in <i>S. cerevisiae, Drosophila</i>, zebrafish, and mice, we discuss how perturbations in RNA surveillance can result in abnormalities in organismal development and homoeostasis. Together, these studies not only enhance our knowledge of the broader relevance of RNA quality control and metabolism but also provide mechanistic insights into pathomechanisms, particularly the tissue-specific vulnerabilities noted in RNA exosome-linked diseases.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"23 1","pages":"1-24"},"PeriodicalIF":4.1,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148219489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic characterization of <i>Actinobacillus pleuropneumoniae</i> serovars 5, 8, and 15 strains from diseased pigs in eastern Chinese provinces.","authors":"Yuanxiu Li, Wenqing Chai, Hang Pan, Weihuan Fang, Huapeng Feng, Jianhong Shu, Yulong He","doi":"10.1080/21505594.2026.2620200","DOIUrl":"10.1080/21505594.2026.2620200","url":null,"abstract":"<p><p><i>Actinobacillus pleuropneumoniae</i> causes porcine infectious pleuropneumonia in pigs. We aimed to characterize the phenotypic and genomic features of three <i>A. pleuropneumoniae</i> strains from clinical cases in eastern Chinese provinces. The serovar 5 strain ZJNH2023 was more pathogenic than strains AH2020 and ZJXS2022 in a murine model and was resistant to multiple antimicrobials. The core genome SNP (single nucleotide polymorphism) tree indicates that the three isolates are clustered with serovars 5, 8, and 15 strains of archived genomes. They harbor plasmids conferring resistance to florfenicol and are of substantial genome diversity, having more prophages, genomic islands (GIs), and antimicrobial resistance genes (ARGs) than the strains of corresponding serovars from other studies. The capsule-related gene clusters in strains AH2022 and ZJXS2022 are different from ZJNH2023 and contain an ISApl1 family transposase between the <i>cps</i> and <i>cpx</i> loci. The serovar 5 strain ZJNH2023 has a full set of <i>ApxI</i> genes, <i>Apa1</i>/<i>Apa2</i>, intact <i>flp</i> family genes related to Flp pilus assembly, and a full set <i>tadABCD</i> genes related to adherence, while strains ZJXS2022 and AH2022 carry <i>ApxIII</i> gene set, lack <i>ApxIAC</i> genes and <i>Apa1/Apa2</i>, and do not have intact <i>flp</i> family genes. Thus, we conclude that possession of the cytotoxic <i>ApxI</i> gene set and those involved in adhesion contributes to higher pathogenicity of the serovar 5 strain ZJNH2023. Distinct GIs and <i>floR</i>-containing plasmids in these strains might have been involved in multiple resistance and horizontal transfer of ARGs on the pig farms.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":" ","pages":"2620200"},"PeriodicalIF":6.8,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12834162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis.","authors":"Linlan Zhou, Jun Liu, Jing Ren, Dehao Du, Xiaofeng Rong","doi":"10.1080/13510002.2026.2646383","DOIUrl":"10.1080/13510002.2026.2646383","url":null,"abstract":"<p><strong>Objectives: </strong>Rheumatoid arthritis (RA) is characterized by chronic synovitis and progressive joint destruction. Ferroptosis has been implicated in RA pathogenesis through synovial iron accumulation and oxidative stress. Glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) are key regulators of ferroptosis, but their specific roles in RA remain incompletely defined. The objective of this research was to explore the therapeutic effects and the mechanisms behind emodin (EMO) in RA.</p><p><strong>Methods: </strong>The therapeutic efficacy and mechanisms of EMO were evaluated in collagen-induced arthritis mice and lipopolysaccharide-stimulated RAW264.7 macrophages. Joint pathology, inflammation, oxidative stress, ferroptosis, and mitochondrial function were analyzed using histology, micro-computed tomography, western blotting, immunohistochemistry, and microscopy. Key targets were identified and validated using molecular dynamics, molecular docking, proteomics, and network pharmacology.</p><p><strong>Results: </strong>EMO alleviated joint inflammation and bone destruction, reduced pro-inflammatory cytokines and oxidative stress, restored iron and mitochondrial homeostasis, and inhibited ferroptosis. Mechanistically, EMO inhibited ferroptosis through the GPX4/ACSL4 axis, as evidenced by increased GPX4 and decreased ACSL4 expression.</p><p><strong>Conclusions: </strong>EMO ameliorates experimental arthritis mainly by suppressing ferroptosis via the GPX4/ACSL4 axis, highlighting ferroptosis as a previously underappreciated therapeutic target in RA and supporting EMO as a potential adjunctive treatment for RA.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2646383"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NOX2/NOX4-associated oxidative stress contributes to G6PD-associated metabolic remodeling and ferroptosis during mice luteolysis.","authors":"Fei Li, JiaHao Song, Wei Zou, Yulu Zhang, YanMin Cheng, HongRu Zhao, Bei Yang, Haibin Kuang","doi":"10.1080/13510002.2026.2724653","DOIUrl":"10.1080/13510002.2026.2724653","url":null,"abstract":"<p><strong>Objective: </strong>Ferroptosis has been shown to participate in luteolysis, yet the upstream signals and metabolic remodeling that trigger it remain unknown. This study aims to clarify these mechanisms.</p><p><strong>Methods: </strong>Physiological postpartum and PGF2α-induced luteolysis models were established in mice. Targeted energy metabolomics, pharmacological inhibition and adenoviral shRNA-mediated knockdown were employed in vivo and in primary luteal cells to measure ferroptosis markers, G6PD activity, NADP⁺/NADPH ratio and NOX2/NOX4 expression.</p><p><strong>Results: </strong>In both models, luteal regression was accompanied by increased ACSL4, decreased GPx4 and GSH, and elevated Fe²⁺ and lipid peroxidation and NOX2 and NOX4 expression. Metabolic analysis revealed 6-phosphogluconate accumulation, reduced pyruvate and pyruvate kinase M activity, and increased G6PD expression and activity, but NADPH depletion and redox imbalance. <i>In vivo</i>, combined NOX2/NOX4 knockdown reduced ROS accumulation, suppressed G6PD hyperactivation, alleviated ferroptotic injuryand delayed regression Moreover, G6PD inhibition with 6-AN similarly reduced oxidative stress and ferroptosis and partially restored progesterone secretion. In primary luteal cells, G6PD knockdown or 6-AN treatment attenuated PGF2α-induced ferroptosis and improved cell viability. Simultaneously, NOX2/NOX4 silencing, N-acetylcysteine, or Ferrostatin-1 suppressed PGF2α-induced G6PD activation, and attenuated oxidative stress and ferroptosis.</p><p><strong>Conclusion: </strong>NOX2/NOX4-associated oxidative stress contributes to G6PD-associated metabolic remodeling and ferroptosis during mice luteolysis.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2724653"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of GSH and H₂S regulation for cancer: an intricate interplay between diet, microbiota, metabolic reprogramming, and immune health.","authors":"Avisek Majumder, Suravi Majumder, Shabana Bano, Koushik Sen, Kasturi Bala Nayak","doi":"10.1080/13510002.2026.2687238","DOIUrl":"10.1080/13510002.2026.2687238","url":null,"abstract":"<p><p>Due to the proliferative nature of cancer cells, they utilize more dietary extracellular nutrients via one-carbon metabolism for the various metabolic processes, including the synthesis of antioxidants such as glutathione (GSH) and hydrogen sulfide (H₂S). Indeed, several studies have found that specific cancer types produce significantly higher levels of GSH and H₂S than normal healthy cells, which may serve as a protective mechanism, allowing them to resist stress, survive, and grow. This metabolic heterogeneity, driven by intrinsic and extrinsic factors, contributes to the distinct metabolic characteristics and vulnerabilities of tumor subtypes, which can be exploited to develop anticancer strategies. In this review, we summarize the fundamental roles and regulation of GSH and H₂S in normal physiological systems and in the genesis and progression of cancer, their effects on the tumor microenvironment (TME), and their contribution to drug resistance. We also discuss the influences of diet and the gut microbiome on GSH and H₂S production, and how cancer cells reprogram their metabolism to grow and survive in a stressful environment by overproducing GSH and H₂S.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2687238"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148227468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRRSV subverts host programmed cell death network for immune evasion.","authors":"Shengming Ma, Qian Mao, Shaoting Weng, Kaiqi Lian, Zhihui Jiang, Jie Hao, Kunpeng Zhang","doi":"10.1080/21505594.2026.2655108","DOIUrl":"10.1080/21505594.2026.2655108","url":null,"abstract":"<p><p>Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen endangering the global swine industry, causing severe reproductive disorders in sows and respiratory diseases in piglets, and incurring substantial economic losses. This review summarizes how PRRSV interferes with multiple programmed cell death (PCD) modalities, including apoptosis, autophagy, pyroptosis, and ferroptosis, thereby optimizing its replication microenvironment, evading host immune responses, and establishing persistent infection. Furthermore, it details the spatiotemporal-specific strategies of PRRSV in regulating PCD during different infection stages and in various cell types, and highlights the pivotal role of virus-host protein interactions in viral pathogenesis. Collectively, this review systematically elucidates the molecular mechanisms by which PRRSV manipulates the host PCD network, and provides crucial theoretical guidance for PRRSV control research and antiviral drug development.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"17 1","pages":"2655108"},"PeriodicalIF":6.8,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the protective role of quercetin against lipopolysaccharide-induced necroptosis in broiler thymus: insights from Nrf2/PERK signaling based on network pharmacology and experimental validation.","authors":"Yu Xia, Ruirui Xie, Xinyu Huo, Kai Chen, Shiping Li, Shiwen Xu, Shu Li","doi":"10.1080/13510002.2026.2663621","DOIUrl":"10.1080/13510002.2026.2663621","url":null,"abstract":"<p><strong>Objectives: </strong>Quercetin (QUE) possesses antioxidant, anti-inflammatory, and immunomodulatory functions. Nuclear factor erythroid 2-related factor 2 (Nrf2) can initiate protein kinase RNA-like ER kinase (PERK), leading to immune dysfunction and necroptosis. Our findings elucidate the therapeutic potential of QUE in attenuating LPS-induced injury in immune tissues.</p><p><strong>Methods: </strong>Broilers and MSB-1 cells were treated with LPS or/and QUE. We also treated MSB-1 cells with an Nrf2 inhibitor (ML385), a PERK activator (MK-28), and a necroptosis inhibitor (NSA) to further explore the detailed mechanism. In addition, we further conducted network pharmacology and bioinformatics to analyze the regulatory relationship between QUE and genes.</p><p><strong>Results: </strong>Combined analysis of network pharmacology and bioinformatics uncovered QUE regulates Nrf2 activation and its crosstalk with PERK signaling, influencing calcium homeostasis, necroptosis, and inflammation. Based on experimental validation, our findings demonstrated QUE treatment reduced LPS-induced imbalance in redox homeostasis through Nrf2 signaling pathway. QUE treatment downregulated the expression of cytokines linked to ERS, necroptosis, and inflammation. In addition, QUE treatment protected against LPS-induced immune function disorders.</p><p><strong>Conclusion: </strong>QUE treatment efficiently attenuated thymus immune disorders and necroptosis in broilers through Nrf2/PERK signaling. This investigation enriches biological function of QUE, providing a solid foundation for developing its potential application.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2663621"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A breast tissue-specific epigenetic clock provides accurate chronological age predictions and reveals de-correlation of age and DNA methylation in tumor-adjacent and tumor samples.","authors":"Leonardo D Garma, Sonia Pernas, Bartomeu Fullana, Andrea Vethencourt, David Vicente Baz, Teresa García Manrique, Rosario García Campelo, Cristina Reboredo, Josefa Terrasa, Antonia Perello, Ramón Colomer, Desirée Jiménez, Ruth Vera García, Susana de la Cruz Sánchez, Begoña Bermejo, Marta Tapia, Santiago González Santiago, Miguel Quintela-Fandino","doi":"10.1080/15592294.2026.2714582","DOIUrl":"10.1080/15592294.2026.2714582","url":null,"abstract":"<p><p>Epigenetic clocks have been widely used to estimate biological age across various tissues, but their accuracy in breast tissue remains suboptimal. Classical models such as Horvath's and Hannum's clocks perform poorly in predicting chronological age in breast tissue, underscoring the need for a tissue-specific approach. In this study, we introduce a Breast Tissue-specific Epigenetic Clock (BTEC), developed using DNA methylation data from 553 healthy breast tissue samples across seven different studies. BTEC significantly outperformed existing clocks, demonstrating superior correlation with chronological age (<i>r</i> = 0.91) and lower prediction errors (MAE = 3.0 y) without requiring dataset-specific regressions adjustments. Notably, BTEC showed consistent performance across ancestry groups, in contrast to existing clocks which exhibited variable ancestry-related biases. We also found that residual-based epigenetic age acceleration, commonly used to correct for prediction bias, is highly dependent on the choice of reference dataset and does not provide a generalizable correction. BTEC's chronological age predictions for tumor-adjacent samples showed distortions, with an average deviation of -2.3 y, which was even more pronounced in tumor samples, where the average difference between predicted and chronological age was -14 to -15 y. When analyzed by molecular subtype, the distortion was greater in the more aggressive HER2+ and TNBC tumors compared to HR+ tumors. Overall, our findings indicate that breast tumors do not generally exhibit accelerated epigenetic aging. The probes used by BTEC were associated with known oncogenes such as JAK1, TP73, PDGFRA, CCND1 and STAT5B, as well as genes involved in cancer-related pathways, including Wnt, Hedgehog and ErbB signaling. Importantly, extreme deviations in epigenetic age, as measured by BTEC-derived epigenetic age acceleration (EAA), were associated with patient survival in HR+ breast cancer patients in an exploratory analysis, highlighting the prognostic value of tissue-specific epigenetic aging measures. These findings demonstrate that BTECs not only improve age prediction in breast tissue but also capture biologically meaningful alterations in tumor epigenetic aging with potential clinical implications.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2714582"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13577255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between RNA secondary and three-dimensional structure prediction: a comprehensive study.","authors":"Deyin Wang, Yangwei Jiang, Linli He, Linxi Zhang, Ruhong Zhou, Dong Zhang","doi":"10.1080/15476286.2026.2655096","DOIUrl":"10.1080/15476286.2026.2655096","url":null,"abstract":"<p><p>In recent years, various computational methods have been developed to predict the three-dimensional (3D) structures of RNAs. Due to its hierarchical folding property, RNA secondary (2D) structure is often used as input for 3D structure prediction to improve accuracy and efficiency. However, the extent to which the accuracy of input 2D structure affects the performance of 3D structure prediction remains to be further investigated. Additionally, whether and how the input base-pairing interactions are modified during the 3D structure modelling process is another question worth exploring. To address these issues, here we comprehensively benchmark six representative 3D structure prediction models on extensive datasets, using 2D structures of varied accuracies as input. Our results indicate that there is a pervasive crosstalk between RNA 2D and 3D structure predictions, where the performance dependence of 3D structure prediction on the accuracy of input 2D structure is closely associated with the 3D model's ability to modify the input base-pairing interactions during structure modelling. Furthermore, we also observed that RNA 3D structure prediction performance is more sensitive to the occurrence of false positive base pairs in the input 2D structure than to true positive base pairs, suggesting a worthy direction to further improve the model performance.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-18"},"PeriodicalIF":4.1,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147594438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}