European journal of cell biology最新文献

{"title":"DAPK1 orchestrates cell division and junction to control corneal epithelial development","authors":"Mulin Yang ,&nbsp;Zihe Zhao ,&nbsp;Weiwen Bu ,&nbsp;Lamei Li ,&nbsp;Xiwen Lin ,&nbsp;Mingzheng Hu ,&nbsp;Dan Dong ,&nbsp;Li Jiao ,&nbsp;Ying Shan ,&nbsp;Min Liu ,&nbsp;Dengwen Li","doi":"10.1016/j.ejcb.2026.151532","DOIUrl":"10.1016/j.ejcb.2026.151532","url":null,"abstract":"<div><div>Stratification of the corneal epithelium plays a vital role in protecting the eye from the external stimuli. However, the molecular mechanisms underlying this process are not fully understood. Herein, we show that death-associated protein kinase 1 (DAPK1) is markedly up-regulated during corneal epithelial development. Exploiting <em>Dapk1</em> knockout mice, we show that depletion of DAPK1 results in corneal opacity and significant thickening of the corneal epithelium. Immunofluorescence staining using epithelial-specific markers reveals that DAPK1 deficiency causes the loss of corneal epithelial properties and the appearance of epidermal-like pathological changes. Further investigation shows that DAPK1 deficiency disrupts corneal epithelial stratification and impairs epithelial cell junctions due to the generation of excessive suprabasal cells through abnormal cell division. Therefore, this study demonstrates a critical role for DAPK1 in the control of corneal epithelial development, indicating DAPK1 as a potential therapeutic target for corneal diseases.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 2","pages":"Article 151532"},"PeriodicalIF":4.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146185127","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":"Integrin β1 mediates mechanosensitive regulation of human trabecular meshwork cell functions in response to substrate stiffness","authors":"Dongyan Li,&nbsp;Ruotian Du,&nbsp;Jilong Li,&nbsp;Yi Xie,&nbsp;Yan Huang,&nbsp;Xianghui Gong,&nbsp;Jing Ji","doi":"10.1016/j.ejcb.2026.151530","DOIUrl":"10.1016/j.ejcb.2026.151530","url":null,"abstract":"<div><div>Increased extracellular matrix (ECM) stiffness is a well-recognized pathological hallmark of the trabecular meshwork (TM) in glaucomatous eyes; however, the mechanotransductive pathways by which TM cells sense and respond to mechanical cues remain incompletely understood. In this study, we identified integrin β1 as a key stiffness-responsive molecule, with its fluorescence signal and membrane localization significantly enhanced in human trabecular meshwork cells (hTMCs) cultured on stiffer substrates. Functional blockade of integrin β1 led to a marked reduction in cell proliferation, migration, and phagocytic activity across all stiffness conditions. Notably, the magnitude of blocking effects varied with substrate stiffness: inhibition of proliferative and migratory capacities was more pronounced on rigid substrates, whereas blockade-induced reduction in phagocytic activity was more evident on compliant substrates. These findings suggest that integrin β1 plays a central role in mediating hTMCs responses to biomechanical signals and may contribute to the functional impairment of the TM outflow pathway in the pathogenesis of glaucoma.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 2","pages":"Article 151530"},"PeriodicalIF":4.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145950248","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":"Polyploid giant cancer cells: A novel target in future cancer therapy","authors":"Guangli Wang ,&nbsp;Hua Wang ,&nbsp;Yuling Wang ,&nbsp;Xi Li ,&nbsp;Heng Luo","doi":"10.1016/j.ejcb.2025.151529","DOIUrl":"10.1016/j.ejcb.2025.151529","url":null,"abstract":"<div><div>Under intense therapeutic stress—including chemotherapy, radiotherapy, and targeted therapies—tumor cells can undergo ploidy reprogramming to generate polyploid giant cancer cells (PGCCs). Once largely overlooked, this rare but biologically distinctive tumor cell subpopulation has now been firmly implicated across multiple malignancies in therapy resistance, metastatic progression, and tumor relapse. PGCCs are characterized by striking morphological and genetic features, including extreme cellular enlargement, multinucleation or high-ploidy states, and profound genomic instability. Importantly, under stress conditions, PGCCs can undergo depolyploidization to produce progeny with enhanced adaptive fitness. This review systematically synthesizes the major mechanisms underlying PGCC formation, including endoreplication, mitotic slippage, cytokinesis failure, cell fusion, and entosis, highlighting their contextual cooperation and temporal continuity across diverse stress environments and genetic backgrounds. We further delineate the core functional roles of PGCCs in tumor biology, with a particular focus on their contributions to therapeutic tolerance, metastasis promotion, and cancer stem cell–like properties, and critically examine their intimate links to intratumoral heterogeneity and tumor evolutionary dynamics. Building on these insights, we evaluate emerging therapeutic strategies targeting PGCCs and discuss current methodological challenges and future directions in their detection, multi-omics characterization, and machine learning–assisted identification.Collectively, PGCCs represent a pivotal stress-adapted cellular state that drives ongoing tumor evolution under therapeutic pressure. A deeper mechanistic understanding of PGCC biology may provide a conceptual framework and novel intervention strategies to overcome cancer resistance and recurrence.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 1","pages":"Article 151529"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911172","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":"Revisiting single-cell migration parameters from 2D video microscopic measurements","authors":"Gréta Bányai ,&nbsp;Márton Bese Naszlady ,&nbsp;János Juhász ,&nbsp;András Horváth ,&nbsp;Balázs Hegedűs ,&nbsp;Tamás Garay","doi":"10.1016/j.ejcb.2025.151524","DOIUrl":"10.1016/j.ejcb.2025.151524","url":null,"abstract":"<div><div>Video microscopy-based single-cell migration analysis allows for precise measurement of cell migration by extracting a range of migration parameters from tracking data during analysis. This study aimed to enhance our understanding of the behavior and sensitivity of these parameters themselves. Random walk simulations and analysis of experimental data were utilized to analyze the sensitivity of migration parameters to tracking methods (manual and semi-automatic), and to assess the repeatability of these parameters. Additionally, the influence of cell line-specific characteristics on migration outcomes was examined.</div><div>Our results demonstrate that displacement-based parameters – mean squared displacement (MSD), displacement (D), and maximal displacement (Max D) – are robust in detecting migration effects but are profoundly influenced by cell line-specific properties, particularly with semi-automatic tracking. These metrics are especially valuable when analyzing data from different, non-identical tracking methods. In contrast, path-based parameters – such as total traveled distance (TTD), velocity (V), and average velocity (AV) – are more sensitive to subtle treatment effects, but are prone to noise from tracking methods and inherently insensitive to treatment-induced changes in directionality.</div><div>Our findings emphasize the importance of combining path-based and displacement-based metrics in video microscopy analyses to achieve a comprehensive picture of cell migration dynamics.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 1","pages":"Article 151524"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665356","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":"Pathogenic podocin variants exhibit distinct defects in trafficking, membrane organization, and degradation pathways","authors":"Pei-Chen Lu ,&nbsp;Ruth Rollason ,&nbsp;Chia-An Chou ,&nbsp;Valeryia Kuzmuk ,&nbsp;Kate J. Heesom ,&nbsp;Moin A. Saleem ,&nbsp;Gavin I. Welsh","doi":"10.1016/j.ejcb.2025.151526","DOIUrl":"10.1016/j.ejcb.2025.151526","url":null,"abstract":"<div><div>Nephrotic syndrome is frequently associated with pathogenic variants in <em>NPHS2</em> (podocin), including the common and severe R138Q substitution. Using conditionally immortalized human podocytes expressing Myc-tagged podocin variants (G92C, V180M, R138Q, R238S, and R291W), we systematically compared variant-specific defects in plasma-membrane trafficking, detergent-resistant microdomain (DRM) localization, and protein stability. All variants displayed reduced plasma membrane abundance and altered DRM distribution. Among them, R138Q-podocin showed uniquely reduced protein stability. Consistent with previous reports, quantitative proteomics revealed a strong enrichment of endoplasmic reticulum (ER) quality-control and ubiquitin–proteasome components in the R138Q interactome, confirming its identity as an ER-associated degradation substrate. Proteasome inhibition with MG132 stabilized R138Q-podocin and restored its trafficking to both the plasma membrane and DRMs, indicating that impaired stability—rather than an intrinsic trafficking defect—restricts its surface localization. Proteomic profiling further identified caveolin-1, CDCP1, and myosin VI as previously unrecognized podocin interactors. These findings expand the podocin interaction network and suggest potential roles in adhesion-associated membrane organization. Collectively, these results demonstrate that pathogenic podocin variants disrupt podocyte function through distinct mechanisms involving degradation, trafficking, and membrane microdomain association, providing insight into variant-specific disease pathways in nephrotic syndrome.</div></div><div><h3>Synopsis</h3><div>This study examined the trafficking, membrane localization, and stability of disease-associated podocin variants. All variants showed reduced plasma-membrane abundance and altered detergent-resistant microdomain distribution, whereas only R138Q-podocin exhibited marked proteasomal degradation. Quantitative proteomics confirmed the endoplasmic reticulum-associated degradation signature of R138Q and identified caveolin-1, CDCP1, and myosin VI as previously unrecognized podocin interactors. These findings reveal variant-specific mechanisms governing podocin stability and membrane organization.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 1","pages":"Article 151526"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788262","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":"Mutations in the Rab33b protein that lead to the skeletal disease Smith-McCort dysplasia result in unstable proteins and altered autophagy function","authors":"Sofia R. Parisi,&nbsp;Danielle Z. Harte,&nbsp;Jeremy C. Simpson","doi":"10.1016/j.ejcb.2025.151528","DOIUrl":"10.1016/j.ejcb.2025.151528","url":null,"abstract":"<div><div>The human skeletal disease Smith McCort dysplasia is known to be caused by mutations in the <em>RAB33B</em> gene. Despite there being detailed genetic and medical studies about the patients carrying these mutated genes, there is a paucity of information about these mutations at the molecular and cellular level. The <em>RAB33B</em> gene encodes the small GTP binding protein Rab33b, which primarily localises to the Golgi apparatus in cells, and plays roles in membrane traffic and autophagy. In recent years, several different mutations in the <em>RAB33B</em> gene have been reported, potentially giving rise to both prematurely truncated proteins and also proteins containing single amino acid substitutions. Importantly, no work to date has examined the consequences of expression of these Rab33b variants in cells. In the study presented here we use a model cell culture system to seek to understand what the consequences might be to cells expressing five of the reported disease-causing Rab33b variants. We specifically examine the ectopic expression of two truncated and three single amino acid substitution variants in cultured cells. Our results reveal that all of these mutants show subcellular mislocalisation and fail to accumulate on Golgi membranes. We also demonstrate that each of these mutants are unstable and suffer from premature degradation in cells. Finally, overexpression of the single amino acid substitution variants in cells induced for autophagy causes a severe reduction in the number of autophagosomes as defined by the number of LC3B-positive puncta. Our results provide the first molecular insight into the cellular effects caused by five of the reported Rab33b mutants that give rise to Smith McCort dysplasia.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 1","pages":"Article 151528"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145921451","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 role of the LOX family in cancer","authors":"Diego Liviu Boaru ,&nbsp;Diego De Leon-Oliva ,&nbsp;Oscar Fraile-Martinez ,&nbsp;Patricia De Castro-Martinez ,&nbsp;Cielo Garcia-Montero ,&nbsp;Connie Ferrara-Coppola ,&nbsp;Majd N. Michael Alhaddadin ,&nbsp;Silvestra Barrena-Blázquez ,&nbsp;Cristina De las Peñas-González ,&nbsp;Noemí Holgado-Tirado ,&nbsp;Mónica Tordesillas-Vicente ,&nbsp;Diego Torres-Carranza ,&nbsp;Laura Lopez-Gonzalez ,&nbsp;Raul Diaz-Pedrero ,&nbsp;Melchor Alvarez-Mon ,&nbsp;Miguel A. Saez ,&nbsp;Miguel A. Ortega","doi":"10.1016/j.ejcb.2025.151527","DOIUrl":"10.1016/j.ejcb.2025.151527","url":null,"abstract":"<div><div>Lysyl oxidase (LOXs) are copper-dependent enzymes traditionally known for catalyzing the cross-linking of collagen and elastin, thereby ensuring extracellular matrix (ECM) stability. However, growing evidence reveals that their biological functions extend far beyond ECM remodeling. This review highlights the diverse roles of the LOX family, comprising LOX, LOXL1, LOXL2, LOXL3, and LOXL4, in tissue repair, vascular remodeling, inflammation, and cancer. Each isoform exhibits unique structural domains, regulatory pathways, and functional interactions with signaling cascades such as TGF-β, PDGF, VEGF, and HIF-1α. LOXs are essential for wound healing, coordinating ECM synthesis and cross-linking during different phases of tissue regeneration. Their expression is tightly modulated by inflammatory cytokines, and their dysregulation has been implicated in pathological fibrosis and impaired tissue repair. In cancer, LOXs contribute to epithelial-to-mesenchymal transition (EMT), cell invasion, and metastasis through both enzymatic and non-enzymatic mechanisms, including intracellular signaling, Snail1 stabilization, and cytoskeletal modulation. They also influence angiogenesis by regulating VEGF expression and promoting endothelial cell activation via PDGFRβ-AKT signaling. Intracellular and nuclear functions further expand their impact on gene regulation and chromatin structure. Given their involvement in matrix dynamics, mechanotransduction, and cell fate determination, LOXs emerge as key players in both physiological and pathological contexts. Understanding their multifactorial roles opens potential avenues for therapeutic targeting in cancer, fibrosis, and chronic inflammatory diseases.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"105 1","pages":"Article 151527"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911155","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 cortical actin cytoskeleton and desmosomes act together in keratin filament network maintenance","authors":"Nicole Schwarz,&nbsp;Sebastian Kant,&nbsp;Rudolf E. Leube","doi":"10.1016/j.ejcb.2025.151516","DOIUrl":"10.1016/j.ejcb.2025.151516","url":null,"abstract":"<div><div>Keratin intermediate filaments are hallmark features of epithelial tissue differentiation forming complex cytoplasmic networks that are connected to subplasmalemmal cortical keratin filaments and anchored at desmosomal junctions. The mechanisms determining keratin filament network morphogenesis and maintenance are poorly understood. We previously generated a homozygous knock-in mouse line expressing YFP-tagged keratin 8, which functionally substitutes for the wild-type keratin 8. 3D time-lapse fluorescence recording of developing pre-implantation embryos allowed monitoring the de novo formation of the keratin filament network, which implicated desmosomes and the actin-rich cell cortex in nucleation and transport of nascent keratin particles. To further explore the relevance of the cell cortex for keratin filament network maintenance, we now studied Krt8-YFP-producing late blastocysts that had developed cytoplasmic and cortical keratin networks. We treated them with drugs to modulate the actomyosin cytoskeleton and analyzed desmosome-deficient blastocysts. We find that overall keratin network organization is barely affected in either scenario. Detailed analyses, however, reveal distinct changes in cytoplasmic keratin filament abundance, cortical anchorage and keratin filament turnover. We conclude that mature keratin networks withstand drastic changes in cellular organization and that maintenance of their spatial organization is secured in a “belt and braces” fashion by multiple mechanisms, notably desmosomal anchorage and attachment to the actin-rich cell cortex.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151516"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145046082","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":"Myosins 1e/f at the podosome base regulate podosome dynamics and promote macrophage migration","authors":"Pasquale Cervero ,&nbsp;Sarah R. Barger ,&nbsp;Perrine Verdys ,&nbsp;Robert Herzog ,&nbsp;Tyler Paul ,&nbsp;Renaud Poincloux ,&nbsp;Stefan Linder ,&nbsp;Mira Krendel","doi":"10.1016/j.ejcb.2025.151514","DOIUrl":"10.1016/j.ejcb.2025.151514","url":null,"abstract":"<div><div>Cells of the monocyte lineage form specialized membrane-associated, actin-rich structures, called podosomes. Podosomes play important roles in cell adhesion and migration as well as the proteolytic degradation of the extracellular matrix. While podosomes are always closely associated with the plasma membrane, the structural components linking the podosome core, composed of branched actin, to the membrane are not fully understood. In this study we show that class I myosins, Myo1e and Myo1f, localize to a specific region of podosomes, underneath the podosome core and near the ventral plasma membrane, and that this localization is mainly mediated by the Myo1e/f TH2 domains. Respective knockdowns or knockouts of Myo1e/f lead to increased podosome size, altered turnover and lateral mobility, which is likely due to Myo1e/f regulating the attachment of core actin filaments to the plasma membrane. In addition, Myo1e/f double knockout macrophages were characterized by a reduction in 3D and 2D migration, even though these cells exhibited increased ability to degrade the extracellular matrix. Along with the other membrane-associated podosome components, such as the transmembrane protein MT-MMP and the GPI-anchored DNase X, Myo1e and Myo1f mark the membrane-proximal region of podosomes. We propose to label this region as the podosome “base”, an additional substructure joining the current trifecta of the podosome cap, core, and ring.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151514"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145027566","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":"Traction-regulated persistence governs durotaxis across cell types","authors":"Hongyuan Zhu ,&nbsp;Xiaoxi Liu ,&nbsp;Jin Wang ,&nbsp;Yunyi Miao ,&nbsp;Yan Liu ,&nbsp;Hui Guo ,&nbsp;Jin Yang ,&nbsp;Zheng Wang ,&nbsp;Tian Jian Lu ,&nbsp;Feng Xu ,&nbsp;Min Lin","doi":"10.1016/j.ejcb.2025.151515","DOIUrl":"10.1016/j.ejcb.2025.151515","url":null,"abstract":"<div><div>Cell migration toward stiffer or softer environments (durotaxis) underlies processes from development to cancer metastasis, yet the underlying mechanism and its universality remain unclear. To resolve this, we investigated how traction forces and directional persistence dictate cell migration along stiffness gradients. We utilized tunable PEG hydrogels with stiffness gradients of 1–16 kPa and perturbed contractility (blebbistatin, oligomycin), and adhesion (vinculin mutants), in cancer cells exhibiting opposing durotactic biases. We found that cells exerting high traction forces migrate persistently towards stiffer regions (positive durotaxis), whereas those with reduced traction lose persistence and shift towards softer regions (negative durotaxis). We developed a computational model linking stiffness-dependent traction from a motor-clutch framework to F-actin stability-driven persistence, capturing both behaviors with one parameter set. The model predicts, and experiments confirm, that tuning myosin activity or adhesion reinforcement can switch durotaxis states. These findings establish a unified mechanism where traction-regulated persistence governs durotaxis bias across cell types. This insight advances design of biomaterials for directed cell migration and suggests therapeutic strategies to control cell trafficking in tissue repair and cancer.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151515"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997253","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}