European journal of cell biology最新文献

{"title":"Deciphering the landscape of post-translational modifications in the centrosome upon T cell activation","authors":"Marta Lozano-Prieto ,&nbsp;Inmaculada Jorge ,&nbsp;Emilio Camafeita ,&nbsp;Cristina A. Devesa ,&nbsp;Rafael Barrero-Rodríguez ,&nbsp;Enrique Calvo ,&nbsp;Andrea Laguillo-Gómez ,&nbsp;Clara Pertusa ,&nbsp;Noa B. Martin-Cofreces ,&nbsp;Jesús Vázquez ,&nbsp;Francisco Sánchez-Madrid","doi":"10.1016/j.ejcb.2025.151521","DOIUrl":"10.1016/j.ejcb.2025.151521","url":null,"abstract":"<div><div>The shift from quiescent to effector T cells (TC) is controlled at the translational level. Post-translational modifications (PTMs) are key factors in the diversification of protein function. Advancements in mass spectrometry-based proteomics enable proteome-wide, hypothesis-free quantitative PTM analysis. Current research highlights the centrosome role in TC activation. Here the diversity of PTMs in the TC centrosome is studied by analyzing centrosome-enriched fractions from human resting and activated T lymphoblasts. Our results show that oxidative modifications predominate in this organelle, with tryptophan as the most frequently oxidized residue. These PTMs are enriched in proteins involved in translation, vesicular trafficking, cytoskeleton organization, among others. We also demonstrate the existence of PTM changes on specific protein regions during TC activation in Myh9 (hyperoxidized), and Gzma (hypoxidized). These hyper- or hypoxidized proteins display distinct functional distributions. Our study provides the first comprehensive PTM mapping of the TC centrosome, underscoring the PTM regulatory role in TC activation.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151521"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226953","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":"Human diamine oxidase undergoes transcytosis and colocalizes with the plasma membrane monoamine transporter indicating intracellular histamine degradation","authors":"Elisabeth Gludovacz ,&nbsp;Grace Wen ,&nbsp;Matthias Weiss-Tessbach ,&nbsp;Felix Kosta ,&nbsp;Gerald Klanert ,&nbsp;Mara Heckmann ,&nbsp;Anna-Lena Hoebler ,&nbsp;Warren L. Lee ,&nbsp;Nicole Borth ,&nbsp;Bernd Jilma ,&nbsp;Thomas Boehm","doi":"10.1016/j.ejcb.2025.151520","DOIUrl":"10.1016/j.ejcb.2025.151520","url":null,"abstract":"<div><div>Secreted human diamine oxidase (hDAO) is the only enzyme capable of extracellular histamine inactivation. Histamine is the key mediator released at high concentrations from activated mast cells causing various unpleasant to life-threatening symptoms. Recombinant hDAO is internalized into various cell types. However, rhDAO-containing intracellular vesicles do not colocalize with the lysosomes indicating that rhDAO is unlikely targeted for direct degradation. After internalization rhDAO was rapidly exocytosed without loss of enzymatic activity and re-internalized. Total internal reflection fluorescence microscopy revealed that rhDAO undergoes transcytosis in endothelial cells. The number of transcytosis events was dose-dependent and saturable indicating a specific, receptor-mediated uptake mechanism. Addition of unlabeled DAO, heparin and heparin-binding motif mutated DAO significantly reduced the number of transcytosis events. After intravenous injection of rhDAO into mice it was detected in vesicles not only within but also below the endothelial cell layer of the thoracic aorta. Localization of hDAO within extracellular vesicles was not detected in biological fluids. In various cell types intracellular vesicular rhDAO colocalized with plasma membrane monoamine transporter (PMAT), but not with the organic cationic transporters 1–3. Histamine is described to be a substrate for all four transporters. Cytoplasmic intravesicular localization of DAO has been detected for many decades but no definite physiological function could be assigned. Newly discovered transcytosis might transport DAO into the interstitial fluid compartment with widespread tissue distribution, especially during pregnancy. Vesicular colocalization of DAO with the histamine transporter PMAT indicates intracellular histamine degradation within these poorly characterized vesicles.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151520"},"PeriodicalIF":4.3,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226955","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":"Structure and function of the keratin 17 tail domain associated with keratin intermediate filament organization","authors":"Jiwoo Yeom ,&nbsp;Sanghoon Lee ,&nbsp;Young Ho Ko ,&nbsp;Eunmi Hong ,&nbsp;Jin Hae Kim ,&nbsp;Pierre A. Coulombe ,&nbsp;Chang-Hun Lee","doi":"10.1016/j.ejcb.2025.151519","DOIUrl":"10.1016/j.ejcb.2025.151519","url":null,"abstract":"<div><div>Keratins are the largest subgroup of intermediate filament proteins, forming 10-nm filaments from type I/II heterodimers, and occur primarily in epithelial cells. Keratin 6 (K6; type II) and Keratin 17 (K17; type I) show a complex expression pattern that includes induction following stress and in several diseases, including carcinomas. K17 is being used as a biomarker for several types of cancer. K6 and K17 sequences are respectively highly homologous to K5 and K14, which are expressed in the progenitor compartment of epidermis and related epithelia. The mechanical support roles of the K6/K17 and K5/K14 pairing require 10 nm filament assembly and the subsequent lateral association of these filaments to form thicker bundles. Previous studies showed that the non-helical tail domain of K14 is dispensable for 10 nm filament assembly but essential to the bundling of K5/K14 filaments. Whether the K6/K17 pairing undergoes bundling, and whether the tail domain of K17 plays a role, is unknown. Here, we use sedimentation assays and electron microscopy to show that, when paired with K6, tailless K17 forms filaments that do not readily bundle. Nuclear magnetic resonance analysis revealed that the isolated K17 tail domain is an intrinsically disordered region (IDR). Follow-up studies with mutant K17 tail constructs suggest that IDR-like tail domains of keratins can form a curved local structure required for bundling and interact dynamically with other regions of keratin filaments in a flexible and heterogeneous manner.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151519"},"PeriodicalIF":4.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225138","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":"PSTPIP1 and pyrin, two key regulators of macrophage differentiation","authors":"Philipp Berger ,&nbsp;Lisa Wilming ,&nbsp;Ricarda Jürgens ,&nbsp;Yevheniia Minchuk ,&nbsp;Sophia Leußink ,&nbsp;Shrey Gandhi ,&nbsp;Carolin Walter ,&nbsp;Sophie-Marie Wind ,&nbsp;Dominik Heider ,&nbsp;Lukas Lamparter ,&nbsp;Milos Galic ,&nbsp;Monika Stoll ,&nbsp;Selina K. Jorch ,&nbsp;Johannes Roth ,&nbsp;Judith Austermann ,&nbsp;Olesja Fehler","doi":"10.1016/j.ejcb.2025.151518","DOIUrl":"10.1016/j.ejcb.2025.151518","url":null,"abstract":"<div><h3>Background</h3><div>Monocytes develop from hematopoietic stem cells; migrate into the tissue, where they undergo a stimulation-dependent and tissue specific differentiation into macrophages imprinting specific inflammatory functions. The development of inflammatory functions during differentiation of progenitor cells into macrophages remained incompletely understood.</div></div><div><h3>Objective</h3><div>We intended to identify regulatory factors driving monocyte/macrophage differentiation.</div></div><div><h3>Methods</h3><div>A Genome-wide CRISPR/Cas9 knockout screen (GeCKO) in ER-HoxB8 macrophages was used to identify key drivers of macrophage differentiation which were verified in independent knock-out and knock-in cells. Immunophenotyping was studied by FACS, morphology and migration by fluorescence microscopy, the inflammatory response by ELISA. Transcriptomic data were obtained by next generation mRNA sequencing and validated by quantitative polymerase chain reaction and immunoblotting.</div></div><div><h3>Results</h3><div>Genome-wide CRISPR/Cas9 knockout screen identified the cytosolic cytoskeleton-associated adaptor molecule PSTPIP1 (proline-serine-threonine phosphatase interacting protein 1) as a regulatory factor of macrophage differentiation. Interestingly, mutations in PSTPIP1 cause autoinflammatory disorders (PAPA syndrome). Deletion of PSTPIP1 resulted in hampered differentiation, decreased inflammatory response, changed morphology, altered cell adhesion and migration properties. PSTPIP1 is a regulator of Pyrin inflammasome activity which drives autoinflammation in familial Mediterranean fever (FMF). Deletion of Pyrin also resulted in a strong alteration of cellular dynamics in macrophages.</div></div><div><h3>Conclusion</h3><div>PSTPIP1 and Pyrin are crucial factors in macrophage differentiation. Their deletion or mutation resulted in a hampered differentiation of macrophages resulting in strong morphological alterations and impacting phagocyte key functions as adhesion and migration. Impaired differentiation of macrophages may represent a significant factor in the pathophysiology of autoinflammatory diseases like FMF and PAPA.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151518"},"PeriodicalIF":4.3,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145118657","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":"A physiologically relevant blood–cerebrospinal fluid barrier model to study the permeability of neurodegenerative biomarkers","authors":"Petra Majerova ,&nbsp;Krutika Khiratkar ,&nbsp;Michaela Skrabanova ,&nbsp;Dominika Olesova ,&nbsp;Lubica Fialova ,&nbsp;Kevin James ,&nbsp;Jozef Vegh ,&nbsp;Juraj Piestansky ,&nbsp;Andrej Kovac","doi":"10.1016/j.ejcb.2025.151517","DOIUrl":"10.1016/j.ejcb.2025.151517","url":null,"abstract":"<div><div>The blood–cerebrospinal fluid barrier (BCSFB) is formed by the choroid plexus and represents the interface between the blood and cerebrospinal fluid (CSF). Several in vitro models have been developed to establish an active cellular barrier and to study the functional and molecular properties of the BCSFB. These models are suitable for simulating disease processes and evaluating drug permeability into brain tissue. Here we have established and optimized a protocol for the high-yield isolation of primary epithelial cells from rat choroid plexus. The addition of cytosine arabinoside suppressed the growth of contaminating cells (fibroblasts and astrocytes), and epithelial culture was grown into a confluent impermeable monolayer within 5–6 days after seeding. To characterize functional and structural properties of our BCSFB model, we employed immunocytochemical and biochemical techniques. Using this model, we assessed the permeability of small molecules as well as proteins associated with neurodegenerative disorders, including tau protein and neurofilament light chain (NfL). The cells were able to secrete cerebrospinal fluid (CSF) actively and the epithelial secretome was enriched in growth factors, cell-matrix proteins, proteases, carrier proteins, and inflammation-related proteins. The novelty of our model lies in its ability to mimic the structural and functional characteristics of the BCSFB while also expressing transporters that are important for pharmaceutical research. The model is suitable for in vitro investigations of the BCSFB, preclinical drug discovery, and for studying the mechanisms by which CNS biomarkers cross from the CSF to the blood during disease.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151517"},"PeriodicalIF":4.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145106449","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":"2025-09-05","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":"2025-09-01","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":"2025-09-01","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}

{"title":"Sterile inflammation in laminopathies","authors":"Rafael Cancado de Faria,&nbsp;Susana Gonzalo","doi":"10.1016/j.ejcb.2025.151512","DOIUrl":"10.1016/j.ejcb.2025.151512","url":null,"abstract":"<div><div>Sterile inflammation, an immune response triggered in the absence of pathogens, plays a key role in various chronic diseases, including aging-related disorders, cancer, and autoimmune conditions. This process is driven by damage-associated molecular patterns, such as self-DNA in the cytosol, which activate innate immune pathways and contribute to persistent inflammation. Chronic activation of these pathways exacerbates tissue damage and accelerates disease progression. Recent studies have connected sterile inflammation to laminopathies, a group of genetic disorders caused by mutations in the <em>LMNA</em> gene, which encodes nuclear intermediate filament proteins essential for nuclear structure and function. In this review we discuss the molecular mechanisms underlying sterile inflammation in laminopathies, emphasizing self-DNA sensing, inflammatory signaling cascade activation, and their pathological consequences. Additionally, we explore potential therapeutic strategies aimed at modulating inflammation and improving disease outcomes. Understanding these interactions may provide new avenues for targeting inflammation in laminopathies and related conditions.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151512"},"PeriodicalIF":4.3,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144921193","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":"Comprehensive in silico analyses of keratin heterodimerisation","authors":"Nicole Schwarz ,&nbsp;Rudolf E. Leube ,&nbsp;Stefan Düsterhöft","doi":"10.1016/j.ejcb.2025.151513","DOIUrl":"10.1016/j.ejcb.2025.151513","url":null,"abstract":"<div><div>Keratins are the largest and most diverse group of intermediate filament proteins, providing structural integrity and mechanical strength to epithelial cells. Although their assembly as heterodimers is well established, the specific pairing preferences and molecular basis of keratin dimerisation remain largely unknown. Here, we employ a high-throughput computational pipeline that integrates AlphaFold Multimer (AFM) modelling, VoroIF-GNN interaction interface quality assessment, interaction energy calculations and structural comparisons with experimentally solved structures to systematically investigate keratin heterodimerisation and to provide a guideline for further analysis of intermediate filament assembly. To validate our in silico approach, we include the well-studied vimentin homodimer as a reference. The predicted vimentin homodimer shows strong agreement with available experimental data, supporting the accuracy of our modelling pipeline. Our results show that keratin heterodimers generally have lower interaction energies, indicating more favourable interactions, than their homodimer counterparts, and exhibit structural configurations that closely resemble known intermediate filament structures. Comparative analyses of different keratin pairs also reveal the importance of the coil 1 region for dimer stability. Furthermore, co-expression of keratin pairings is demonstrated by analysis of spatial transcriptomics data in skin under physiological and pathological conditions. Collectively, these findings highlight structural principles underlying canonical keratin heterodimerisation and establish a robust computational workflow for elucidating alternative keratin dimerisations.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 4","pages":"Article 151513"},"PeriodicalIF":4.3,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997254","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}