Cell Biology International最新文献

{"title":"Orchestrating Microtubules: A Review of Kinase–Dependent Regulatory Mechanisms","authors":"Yaqian Zhang,&nbsp;Shasha Hua,&nbsp;Kai Jiang","doi":"10.1002/cbin.70133","DOIUrl":"10.1002/cbin.70133","url":null,"abstract":"<div>\u0000 \u0000 <p>Microtubules are subject to dynamic regulation through post-translational modifications, with phosphorylation serving as a key mechanism. The human kinome, comprising over 500 protein kinases, represents a comprehensive regulatory network. Some of these kinases precisely regulate microtubule dynamics and organization, both spatially and temporally, by modulating various microtubule-associated proteins or by directly binding to microtubules. This review, based on a systematic and kinome-wide perspective across multiple physiological systems, provides a comprehensive overview and in-depth analysis of the key kinase families that regulate microtubules, covering both direct and indirect mechanisms. The complex interactions between these kinases and microtubules are not only vital for normal cellular physiology but are often disrupted in various diseases, particularly cancer and neurodegenerative disorders. By synthesizing this knowledge, our work enhances the understanding of kinase–mediated microtubule regulation and lays a foundation for the future development of targeted therapeutic strategies.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146040630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RFC4 Promotes the Metastasis of Colorectal Cancer by Regulating the Wnt/β-Catenin Pathway","authors":"Guansheng Hu,&nbsp;Laiai Fang,&nbsp;Xiang Ding,&nbsp;Qingjun Zeng,&nbsp;Youwu Wen,&nbsp;Dongyang Cheng,&nbsp;Yonggui Zhou","doi":"10.1002/cbin.70136","DOIUrl":"10.1002/cbin.70136","url":null,"abstract":"<div>\u0000 \u0000 <p>Replication factor C (RFC), a multimeric protein with ATPase activity, plays a crucial role in DNA replication and repair. RFC4, one of its subunits, is aberrantly expressed in various malignant tumors, including colorectal cancer (CRC). Nevertheless, the impact of RFC4 on CRC metastasis remains to be elucidated. In this study, we systematically examined the effects of RFC4 silencing on the proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and Wnt/β-catenin signaling pathway in CRC cells in vitro. Additionally, we further explored the regulatory role of RFC4 in liver metastasis of CRC cells in vivo. Finally, BML-284, a known activator of the Wnt/β-catenin signaling pathway, was employed to validate the underlying mechanism by which RFC4 modulates the invasive phenotype of CRC cells. The results demonstrated that RFC4 was significantly overexpressed in CRC cell lines. Upon silencing of RFC4, the proliferation, migration, and invasion capabilities of CRC cells were markedly attenuated, and the EMT process as well as Wnt/β-catenin signaling pathway activity were effectively suppressed. Notably, RFC4 silencing significantly reduced liver metastasis of CRC cells in a nude mouse model. However, the inhibitory effects of RFC4 silencing on CRC cells proliferation, migration, invasion, and EMT were partially reversed by the intervention of the Wnt/β-catenin signaling pathway activator BML-284. Altogether, these results indicate that RFC4 plays a critical role in promoting CRC metastasis, and its mechanism of action may involve the regulation of Wnt/β-catenin signaling pathway activation to facilitate EMT.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A-Mediated IGF1 Hypomethylation Impairs Decidualization and Promotes Preeclampsia Pathogenesis: Implications for Epigenetic Therapy","authors":"Jing Tong,&nbsp;Xingyun Yan,&nbsp;Cong Zhang","doi":"10.1002/cbin.70137","DOIUrl":"10.1002/cbin.70137","url":null,"abstract":"<div>\u0000 \u0000 <p>The decidua, a dynamic and heterogeneous maternal tissue essential for pregnancy maintenance, has emerged as a key contributor to preeclampsia (PE) pathogenesis. Using methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq), we profiled N6-methyladenosine (m⁶A) methylation patterns and mRNA expression in the decidua of early-onset PE (EPE), late-onset PE (LPE), and normal pregnancy (NP) samples. Integrated analysis revealed that differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were significantly enriched in pathways critical for decidualization, including HIF-1, PI3K-AKT, and Rap1 signaling. These pathways exhibited concurrent m⁶A methylation and expression changes, implicating their involvement in PE development. Notably, insulin-like growth factor (IGF1) was hypomethylated and downregulated in PE decidua compared to NP controls. Given IGF1's central role in stromal cell differentiation and decidualization, its dysregulation likely impairs normal decidual function. Validation using external datasets, quantitative PCR, and siRNA knockdown in human endometrial stromal cells confirmed reduced IGF1 expression and its impact on decidual markers like prolactin. Our findings demonstrate that disrupted m⁶A methylation impairs decidualization via IGF1 regulation, offering novel mechanistic insight into PE. This study highlights the importance of epitranscriptomic regulation at the maternal-fetal interface and identifies m⁶A-modified transcripts as potential therapeutic and diagnostic targets in PE.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Autophagy Regulates the Apoptosis of Bone Marrow-Derived Mesenchymal Stem Cells Under Hypoxic Condition via AMP-Activated Protein Kinase/Mammalian Target of Rapamycin Pathway","authors":"","doi":"10.1002/cbin.70135","DOIUrl":"10.1002/cbin.70135","url":null,"abstract":"<div>\u0000 \u0000 <p><b>RETRACTION:</b> Z. Zhang, M. Yang, Y. Wang, L. Wang, Z. Jin, L. Ding, L. Zhang, L. Zhang, W. Jiang, G. Gao, J. Yang, B. Lu, F. Cao, and T. Hu, “Autophagy Regulates the Apoptosis of Bone Marrow-Derived Mesenchymal Stem Cells Under Hypoxic Condition via AMP-Activated Protein Kinase/Mammalian Target of Rapamycin Pathway,” <i>Cell Biology International</i> 40, no. 6 (2016): 671–685. https://doi.org/10.1002/cbin.10604.</p>\u0000 <p>The above article, published online on 23 March 2016 in Wiley Online Library (wileyonlinelibrary.com), and its correction (https://doi.org/10.1002/cbin.12142), have been retracted by agreement between the journal Editorial Board, Xuebiao Yao; and John Wiley &amp; Sons Ltd. An investigation by the publisher found several image duplications from other previously published articles: The beta-actin band in Figure 3 C includes overlapping blot sections that appear in an article by different authors [Li et al. 2013 (https://doi.org/10.1371/journal.pone.0076689)]. The AMPK bands in Figure 4 A was duplicated and manipulated from another article by different authors [Peng et al. 2013 (https://doi.org/10.1371/journal.pone.0079739))]. The DAPI Hypoxia/SD + , 3-MA-, Rapamycin+ image in Figure 6 A was duplicated from another article by different authors [Zhang et al. 2013 (https://doi.org/10.1371/journal.pone.0080342]. The investigation also found evidence of duplication between the second and fourth LC3-I bands in Figure 5D. In addition, a third party reported that an article by some of the same authors re-used and manipulated images that also appear in this article [Yang et al. 2018 (https://doi.org/10.1186/s13287-018-1028-5)]. Lastly, the investigation found that the DAPI Hypoxia/SD + , 3-MA-, Rapamycin- image in Figure 6 A also appears in a later article by different authors [Chen et al. 2018 (https://doi.org/10.1159/000488117)].</p>\u0000 <p>The authors responded to an inquiry by the publisher and shared original data. A review of their response and the original data found that the explanations for image duplication from previously published articles and within the article were not adequate to explain the identified concerns.</p>\u0000 <p>A correction to this article had been published previously on 11 March 2024 (https://doi.org/10.1002/cbin.12142) which replaced multiple images in Figure 5 A and the “Normal” image in Figure 7 F due to errors in those figures. However, the additional concerns in Figures 3, 4, and 6 cast doubt on the accuracy of the data presented in the article. The retraction has been agreed to because the image duplication and manipulation identified have fundamentally compromised the editors' confidence in the results and conclusions presented in the article. The authors disagree with the retraction.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017666","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":"Engineering Immortalized Bovine Granulosa Cells Using a Triple-Gene Approach: Mutant CDK4, Cyclin D1, and TERT","authors":"Lanlan Bai,&nbsp;Minami Takahashi,&nbsp;Jin Kobayashi,&nbsp;Takahiro Eitsuka,&nbsp;Himari Matsusaka,&nbsp;Taku Ozaki,&nbsp;Eriko Sugano,&nbsp;Hiroshi Tomita,&nbsp;Yuan Xu,&nbsp;Kazuhiro Kawamura,&nbsp;Kiyotaka Nakagawa,&nbsp;Tohru Kiyono,&nbsp;Tomokazu Fukuda","doi":"10.1002/cbin.70126","DOIUrl":"10.1002/cbin.70126","url":null,"abstract":"<p>Advancing reproductive technologies in livestock is essential to improve both productivity and genetic potential of cattle. Despite this importance, application of reproductive biotechnologies in cattle breeding remains limited. Bovine granulosa cells (bGCs), which are key components of the ovarian follicle, are critical in female reproduction as they produce steroid hormones and growth factors necessary for oocyte development. However, primary bGCs exhibit restricted proliferative capacity in vitro, limiting their utility in large-scale studies on mechanisms related to follicular development. To address this limitation, we attempted to immortalize bGCs by co-expressing human mutant cyclin-dependent kinase 4 (CDK4^R24C), cyclin D1, and telomerase reverse transcriptase (TERT) using lentiviral vectors. The resulting immortalized cells (bGCs-K4DT) displayed extended proliferative lifespans, surpassing 100 population doublings without exhibiting signs of senescence. The transduced cells demonstrated a more active cell cycle profile and higher telomerase activity relative to parental bGCs. Importantly, they retained the bGC-specific marker, aromatase, albeit at reduced expression levels. This immortalized bGC offers a promising model for investigating the role of bioactive components of platelet-rich plasma (PRP) in follicular activation and growth, thereby supporting innovations in livestock reproductive technologies.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008622","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":"Solute Carrier Family 19 Member 1 Mediates Acquired Bortezomib Resistance in Multiple Myeloma Through Chronic Stimulator of Interferon Genes Activation and Mitochondrial DNA Release","authors":"Yixuan Chen,&nbsp;Xianyi Wu,&nbsp;Mingxuan Tang,&nbsp;Xin Li,&nbsp;Xiaotao Wang","doi":"10.1002/cbin.70130","DOIUrl":"10.1002/cbin.70130","url":null,"abstract":"<div>\u0000 \u0000 <p>Acquired drug resistance is a major cause of poor prognosis in multiple myeloma (MM). Bortezomib (BTZ), a first-line therapeutic agent, is highly effective in MM; however, resistance remains a significant clinical challenge. Our previous work implicated Solute Carrier Family 19 Member 1 (SLC19A1) in hypoxia and immune modulation, suggesting its potential role in malignant progression. Here, we found that SLC19A1 expression was elevated in MM patients, particularly in those with acquired resistance. Overexpression of SLC19A1 enhanced the proliferation and invasiveness of human myeloma cell lines but did not confer primary BTZ resistance. Using a continuous-BTZ-exposure model, we demonstrated that SLC19A1 overexpression mediated acquired resistance via chronic activation of the stimulator of interferon genes (STING) pathway. This sustained activation triggered the unfolded protein response, dysregulated the endoplasmic reticulum–mitochondrial axis, and induced mitochondrial DNA (mtDNA) release. Treatment with the SLC19A1 inhibitor sulfasalazine or the STING inhibitor H-151 reduced mtDNA release and restored BTZ sensitivity. These findings highlight SLC19A1 and STING signaling as potential therapeutic targets for overcoming acquired drug resistance in MM.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The miR-148/152 Family Suppresses Apoptosis and Necroptosis for Cancer Evasion Through Direct RIPK1 Repression","authors":"Jingjing Li,&nbsp;Qiuye Li,&nbsp;Yuting Ji,&nbsp;Cong Zhao,&nbsp;Yayun Du,&nbsp;Sudan He,&nbsp;Xiaoliang Yu","doi":"10.1002/cbin.70131","DOIUrl":"https://doi.org/10.1002/cbin.70131","url":null,"abstract":"<div>\u0000 \u0000 <p>Evasion of programmed cell death, including apoptosis and necroptosis, is a critical hallmark of cancer that contributes to tumorigenesis and chemoresistance. While microRNAs (miRNAs) are known to modulate cell death pathways, the role of specific miRNA families in coordinated death resistance remains incompletely understood. Through functional screening, we identified the miR-148/152 family as potent suppressors of tumor necrosis factor (TNF)-induced cell death, prompting an investigation into their regulatory mechanism in both apoptosis and necroptosis and their oncogenic role. Ectopic expression of miR-148a or miR-152 inhibits TNF-induced apoptosis and necroptosis in multiple human cancer cell lines, accompanied by reduced activation of caspase-8, caspase-3, RIPK1, and RIPK3. Mechanistically, the miR-148/152 family directly target the 3′UTR of RIPK1, which is a critical regulator in TNF-mediated cell death, thus downregulating its expression. Functionally, miR-152 enhances cancer cell proliferation and colony formation. Clinically, high expression of miR-152 correlates with poor prognosis in gastric cancer patients. Importantly, this miRNA confers resistance to cisplatin-induced, RIPK1-mediated cell death, promoting gastric cancer cell survival and proliferation. Our study defines the miR-148/152 family as critical oncogenic drivers that promote cancer cell survival and chemoresistance by directly suppressing RIPK1 expression. These findings highlight this miRNA family as a promising therapeutic target to overcome cell death evasion in cancer.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146007736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD44 N-Glycosylation Alleviates Myocardial Ischemia–Reperfusion Through PI3K/AKT/mTOR Pathway","authors":"Yanxin Ren,&nbsp;Haibin Dong,&nbsp;Qingwen Huang,&nbsp;Bowen Xu,&nbsp;Kaixuan Fu,&nbsp;Jikai Song,&nbsp;Lei Gong,&nbsp;Yiming Wang,&nbsp;Xiaoning Ding,&nbsp;Lin Zhong,&nbsp;Jun Yang,&nbsp;Wenjuan Jia","doi":"10.1002/cbin.70132","DOIUrl":"10.1002/cbin.70132","url":null,"abstract":"<div>\u0000 \u0000 <p>Myocardial ischemia–reperfusion injury (MIRI) is one of the leading causes of morbidity and mortality from cardiovascular diseases worldwide. Protein N-glycosylation plays an important role in MIRI. However, there is limited knowledge regarding N-glycoproteins in MIRI and their alterations during MIRI. This study aims to investigate the dynamic changes of N-glycosylation modification in MIRI and the regulatory mechanisms of key proteins in MIRI to provide new therapeutic targets for the clinical diagnosis and treatment of MIRI. This study systematically explored the dynamic changes of N-glycosylation modification in MIRI through an integrated glycoproteomic analysis, combining a clinical sample, animal models, and cell models. Differential glycoproteins were identified using quantitative N-glycoproteomic mass spectrometry. Key regulatory molecules were screened through GO functional annotation and KEGG pathway enrichment. The integrated analysis identified 698 N-glycosylated proteins. Pathway enrichment analysis showed that the differentially expressed proteins were mainly involved in the PI3K/AKT/mTOR signaling pathway. The study of differentially expressed N-glycoproteins revealed that CD44 was upregulated and could regulate AKT. One possible reason is that N-glycosylation of CD44 affects its stability.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrachlorobisphenol A Induces Programmed Cell Death and Senescence in Vascular Endothelial Cells","authors":"Huanyu Qiao,&nbsp;Bo Yang,&nbsp;Xiaoshuo Lv,&nbsp;Yongmin Liu","doi":"10.1002/cbin.70121","DOIUrl":"10.1002/cbin.70121","url":null,"abstract":"<div>\u0000 \u0000 <p>Tetrachlorobisphenol A (TCBPA) is an organic compound extensively utilized in industrial production as an alternative to Tetrabromobisphenol A (TBBPA). Currently, TCBPA has been frequently detected in various environmental media. TCBPA residues have been detected in environmental samples, prompting concerns about its potential toxicological impact on human health. This study focuses on the potential impact of TCBPA on vascular health, particularly its effects on vascular endothelial cells. Through CCK8 and EdU assays, we observed that TCBPA treatment inhibited the proliferation of vascular endothelial cells. Further studies showed that TCBPA triggers an inflammatory response in vascular endothelial cells, including IL-6, IL-1β, and TNF-α. Additionally, TCBPA was found to trigger oxidative stress in vascular endothelial cells, as evidenced by increased levels of reactive oxygen species (ROS). Further studies demonstrated that TCBPA led to programmed necrosis and senescence in vascular endothelial cells. Mechanistically, we discovered that ROS-induced mitochondrial Z-DNA played a critical role in this process. Our findings suggest that TCBPA may inhibit vascular endothelial cell proliferation, posing a potential risk for vascular damage. This study highlights the importance of regulating TCBPA usage to minimize potential health risks.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “C/EBPβ Enhances Efficacy of Sorafenib in Hepatoblastoma”","authors":"","doi":"10.1002/cbin.70128","DOIUrl":"https://doi.org/10.1002/cbin.70128","url":null,"abstract":"<p>Pang, C., Miao, H., Zuo, Y., Guo, N., Sun, D., &amp; Li, B. (2021). C/EBPβ enhances efficacy of sorafenib in hepatoblastoma. <i>Cell Biol Int</i>, 45, 1897–1905, https://doi.org/10.1002/cbin.11624</p><p>In the originally published article, the Funding Information section was incomplete due to the inadvertent omission of a grant. The complete and corrected Funding Information section should read as follows:</p><p>Funding information</p><p>The Natural Science Foundation of Hebei province, Grant/Award Number: H2021406043; 2021 Research Start-up Fund for High-level Talents of Chengde Medical College, Grant/Award Number: 202109; Science and Technology Research and Development Program of Chengde, Grant/Award Number: 201904A097; the school private research management of Chengde Medical University, Grant/Award Numbers: 201814, 202004.</p><p>We apologize for this error.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146002238","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}