The EMBO JournalPub Date : 2026-04-28DOI: 10.1038/s44318-026-00788-y
Chao Wei,Jun Sun,Zhuoyan Liu,Mulan Wang,Jin Tan,Xiaona Huang,Ranran Dai,Kang Su,Shiwen Yang,Tara S R Chen,Qi Tian,Xiuxiao Tang,Xiaolin Tian,Dong-Feng Huang,Jin Bai,Xue Xiao,Xiaoting Shen,Juan Xia,Junjun Ding,Lili Fan
{"title":"RYBP regulates selective genomic binding of TrxG and PcG components in embryonic stem cell fate control.","authors":"Chao Wei,Jun Sun,Zhuoyan Liu,Mulan Wang,Jin Tan,Xiaona Huang,Ranran Dai,Kang Su,Shiwen Yang,Tara S R Chen,Qi Tian,Xiuxiao Tang,Xiaolin Tian,Dong-Feng Huang,Jin Bai,Xue Xiao,Xiaoting Shen,Juan Xia,Junjun Ding,Lili Fan","doi":"10.1038/s44318-026-00788-y","DOIUrl":"https://doi.org/10.1038/s44318-026-00788-y","url":null,"abstract":"Selective gene expression is pivotal in orchestrating human development. Specifically, trithorax group (TrxG) and polycomb group (PcG) components play crucial roles in transcriptional activation and repression of state-specific stem cell expression programs, yet the mechanisms underlying their selective genomic binding remain poorly understood. In this study, we report that the polycomb repressive complex 1 (PRC1) subunit RYBP co-localizes with TrxG component WDR5 and selectively enriches PcG component RING1B in condensates in murine embryonic stem cells (ESCs). RYBP deficiency impairs the genomic binding of WDR5 and RING1B. Further, STAT3 excludes RING1B binding at RYBP-associated transcriptionally active loci. Additionally, RYBP depletion attenuates WDR5-dependent activation of DNA repair gene expression and facilitates the transition of ESCs to 2-cell-like cells. Finally, RYBP depletion disrupts RING1B deposition at lineage-specific genes, promoting ESC differentiation towards mesendoderm fate. These findings uncover RYBP as a regulator of selective genomic binding of TrxG and PcG components, providing insights into their roles in cell fate determination during development.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147754700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2026-04-24DOI: 10.1038/s44318-026-00775-3
Laura-Yvonne Gherghina,Jocelyn L Y Tang,Leo Otsuki,Leia Judge,Andrea H Brand
{"title":"Quiescent neural stem cells transiently become neuron-like to coordinate long-range reactivation.","authors":"Laura-Yvonne Gherghina,Jocelyn L Y Tang,Leo Otsuki,Leia Judge,Andrea H Brand","doi":"10.1038/s44318-026-00775-3","DOIUrl":"https://doi.org/10.1038/s44318-026-00775-3","url":null,"abstract":"Reactivation of quiescent neural stem cells (NSCs) in the central nervous system (CNS) is a tightly controlled process that generates new neurons and glia to maintain homeostasis or enable repair post-injury, but it remains unclear if reactivation of distinct NSC populations is coupled. Here, we discovered that NSC quiescence exit in Drosophila follows a hierarchical sequence, whereby activation of anterior stem cells in the brain lobes precedes and is required for the timely state-transition of more posterior NSCs in the ventral nerve cord. To achieve this, quiescent NSCs transiently activate neuronal genes. This transient neuronal state is temporary and specific to NSC dormancy, as neuronal genes are switched off after stem cells resume proliferation. Blocking neuronal firing in brain lobe neurons delays the onset of posterior NSC reactivation. Our results reveal long-range communication between quiescent NSCs to coordinate reactivation across the CNS, enabled by a transient, plastic neuron-like state that allows direct interaction with neuronal axons.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"244 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tissue-selective COPII modulator SEC16B aggravates cardiovascular disease by promoting lipid export.","authors":"Xiao Wang,Yating Hu,Lu Liu,Runze Huang,Yawei Wang,Bing Liu,Yifei Zhao,Yuangang Zhu,Jia Lv,Liang Liu,Huimin Wang,Lingzhi Wu,Xinxuan Xu,Yaxin Li,Guanlin Wang,Xiao-Wei Chen","doi":"10.1038/s44318-026-00754-8","DOIUrl":"https://doi.org/10.1038/s44318-026-00754-8","url":null,"abstract":"The biogenesis and transport of lipoproteins are essential for systemic homeostasis and cardiometabolic health, yet how the secretory pathway acquires specialization to support high-capacity lipoprotein export remains unclear. Here, we report SEC16B as a tissue-selective modulator of the COPII machinery, critical for the efficient secretion of APOB-containing lipoproteins. Integrative bioinformatic analyses identify that SEC16B co-emerges with core genes involved in lipoprotein biogenesis. Functional studies, coupled with AI-driven prediction, reveal that SEC16B acts as a molecular brake to fine-tune COPII condensation for lipoprotein export. Mining of UK biobank data links SEC16B to metabolic traits in humans and suggests HNF4A-dependent regulation of SEC16B expression. Hepatic deletion of SEC16B in mice markedly reduces circulating APOB, triglycerides and cholesterol, while conferring robust protection against atherosclerosis and cardiac dysfunction and maintaining liver health. Collectively, these findings position SEC16B as a specialized modulator of lipoprotein export via the general secretory (SEC) pathway in the liver, suggesting potential therapeutic avenues for combating cardiometabolic diseases.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2026-04-22DOI: 10.1038/s44318-026-00776-2
Pooneh Koochaki,Biao Qiu,Jesse A Coker,Alexander Earsley,Nancy S Wang,Todd Romigh,Christopher M Goins,Carleigh Salem,Dehui Mi,Emily Days,Joshua A Bauer,Shaun R Stauffer,Olga Boudker,Abhishek A Chakraborty
{"title":"Structure-guided optimization of SLC1A1/EAAT3-selective inhibitors targeting renal cancer metabolism.","authors":"Pooneh Koochaki,Biao Qiu,Jesse A Coker,Alexander Earsley,Nancy S Wang,Todd Romigh,Christopher M Goins,Carleigh Salem,Dehui Mi,Emily Days,Joshua A Bauer,Shaun R Stauffer,Olga Boudker,Abhishek A Chakraborty","doi":"10.1038/s44318-026-00776-2","DOIUrl":"https://doi.org/10.1038/s44318-026-00776-2","url":null,"abstract":"Renal cell carcinomas (RCCs) depend on the trimeric sodium-coupled aspartate and glutamate transporter, SLC1A1/EAAT3; however, pharmacologically targeting SLC1A1 is challenging. Here we determined a cryo-EM structure of human SLC1A1 bound to compound 3e, a recently described SLC1A1-selective bicyclic imidazo[1,2 α]pyridine-3-amine (BIA) inhibitor with an unclear mechanism of action. 3e binds a membrane-embedded allosteric pocket accessible only in the apo state, when SLC1A1 is unbound to substrate and sodium, and likely prevents sodium and substrate binding. Moreover, by forming a wedge between the trimerization domain and the substrate-binding transport domain, alongside a cholesterol moiety from the lipid bilayer, 3e blocks SLC1A1's elevator-like movements that support the transport cycle. Mutations in this binding pocket abolish the 3e interaction and counteract 3e's cytotoxicity in RCC cells, confirming on-target activity and explaining SLC1A1 selectivity. The subsequent design of two new SLC1A1-selective BIA derivatives, PBJ1 and PBJ2, was directed by the SLC1A1-3e structures; both inhibited SLC1A1-dependent aspartate, glutamate, and cysteine metabolism and showed enhanced cytotoxicity.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"65 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147733771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"T-cell protrusions enable fast, localised initiation of chimeric antigen receptor signalling.","authors":"Carmen Rodilla-Ramirez,Giorgia Carai,Eleanor Fox,Amin Zehtabian,Helen Adam,Katja Dallio,Pia Lazki-Hagenbach,Helge Ewers,Xiaolei Su,Francesca Bottanelli","doi":"10.1038/s44318-026-00773-5","DOIUrl":"https://doi.org/10.1038/s44318-026-00773-5","url":null,"abstract":"Actin-rich protrusions densely cover the surface of T cells and are well characterised for their role in migration. Recent studies have uncovered their contribution to antigen surveillance and immune signalling. To further explore how protrusions initiate signalling pathways mediating T-cell activation, we performed live-cell imaging of endogenously tagged proteins in HER2-specific chimeric antigen receptor (CAR) T cells targeting HER2⁺ breast-cancer cells. Quantitative STED microscopy allowed us to monitor protein rearrangement and to correlate it with membrane topology over time. Before activation, key signalling proteins (including Lck, CD45, LAT, and the CAR) were not enriched in protrusions. Upon contact with target cells, rapid protein reorganisation occurred preferentially within protrusions, initiating signalling. HER2-CAR clustering, accompanied by ZAP-70 and LAT recruitment, was enhanced in protrusions. While Lck distribution remained unchanged, exclusion of the phosphatase CD45 was enhanced at protrusion-cell contacts, independently of the CAR signalling domain. Overall, signalling machinery rearranged faster and more effectively at protrusive contacts than at main plasma membrane regions. Together, our data re-frame protrusions as sites of enhanced receptor activation by exclusion and clustering dynamics rather than by pre-enrichment of the signalling machinery.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"135 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2026-04-21DOI: 10.1038/s44318-026-00780-6
Eishi Aizawa,So Shimamoto,Eriko Kajikawa,Junko Hara,Takaya Abe,Hiroki Shibuya,Tomoya S Kitajima
{"title":"Dynamic blebbing and absence of organelle transfer during mouse oocyte formation.","authors":"Eishi Aizawa,So Shimamoto,Eriko Kajikawa,Junko Hara,Takaya Abe,Hiroki Shibuya,Tomoya S Kitajima","doi":"10.1038/s44318-026-00780-6","DOIUrl":"https://doi.org/10.1038/s44318-026-00780-6","url":null,"abstract":"Oocyte formation in mammals is a tightly regulated process essential for female fertility, yet the underlying mechanisms remain poorly understood. In this study, we establish an ex vivo culture system that faithfully recapitulates in vivo development and enables long-term live imaging of mouse fetal ovaries. Using high resolution imaging, we capture the dynamic behaviors of germ cells during the development from oogonia to nascent oocytes. We identify pronounced blebbing activity during the mitosis-to-meiosis transition. This behavior is regulated by meiotic initiation signals, underscoring its potential developmental relevance, although its precise role remains unclear. A prevailing model suggests that oocyte formation involves organelle transfer from neighboring germ cells during cyst breakdown. However, through photoconversion-based tracking, we observe no detectable transfer of mitochondria or centrosomes, as organelles remain confined to individual cells. These findings point to alternative mechanisms for cytoplasmic enrichment in oocytes. Our study provides new insights into mammalian oocyte formation and establishes a powerful platform for analyzing germ cell dynamics in real time.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CD20 tails interact with the 14-3-3/GEF-H1 complex and microtubule network upon PKCδ phosphorylation.","authors":"Kathrin Kläsener,Cindy Eunhee Lee,Julian Bender,Angela Naumann,Lena Reimann,Geoffroy Andrieux,Claudio Mussolino,Nadja Herrmann,Roland Nitschke,Reinhard E Voll,Bettina Warscheid,Klaus Warnatz,Michael Reth","doi":"10.1038/s44318-026-00781-5","DOIUrl":"https://doi.org/10.1038/s44318-026-00781-5","url":null,"abstract":"CD20 is a four-helix transmembrane protein specifically expressed in B-cells that serves as a prominent target of therapeutic anti-CD20 antibodies. It is localized in a membrane nanocluster harboring the B-cell antigen receptor of IgD class (IgD-BCR), where it functions to maintain the resting state of naïve B-lymphocytes. How CD20 exerts this resting B-cell gatekeeper function is not yet known. Using Ramos and human peripheral blood B-cells, we show here that the serine/threonine kinase PKCδ constitutively phosphorylates serine residues in the two cytosolic tails of CD20. Phosphorylated CD20 becomes a binding target for 14-3-3 adaptor proteins, which link it to the RhoA GDP/GTP exchange factor GEF-H1 and the microtubule network, supporting the function of the IgD-BCR nanocluster. Binding of anti-CD20 antibodies results in microtubule dissociation and replacement of the GEF-H1/CD20 complex with a RhoA-GTP/ROCK1/CD20 complex, which promotes actomyosin contractility. Our study suggests that CD20 not only maintains the resting state of B-lymphocytes by anchoring the microtubule network and controlling the stability of the IgD-BCR nanocluster, but also mediates the microtubule/actin switch in active B-lymphocytes. These findings could have important implications for anti-CD20 antibody treatment and the optimization of therapeutic protocols.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"242 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147702132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2026-04-16DOI: 10.1038/s44318-026-00774-4
Antonella F M Dost,Katarína Balážová,Carla Pou Casellas,Lisanne M van Rooijen,Wisse Epskamp,Gijs J F van Son,Willine J van de Wetering,Carmen Lopez-Iglesias,Harry Begthel,Peter J Peters,Niels Smakman,Johan H van Es,Hans Clevers
{"title":"Interferon-γ selectively promotes survival of alveolar progenitor cells in a human lung organoid model.","authors":"Antonella F M Dost,Katarína Balážová,Carla Pou Casellas,Lisanne M van Rooijen,Wisse Epskamp,Gijs J F van Son,Willine J van de Wetering,Carmen Lopez-Iglesias,Harry Begthel,Peter J Peters,Niels Smakman,Johan H van Es,Hans Clevers","doi":"10.1038/s44318-026-00774-4","DOIUrl":"https://doi.org/10.1038/s44318-026-00774-4","url":null,"abstract":"Disease of the lung alveoli is frequently associated with acute or chronic inflammation. At present, there are no effective therapies to support regeneration of the alveolar epithelium, and ongoing inflammation adds an additional layer of complexity to many lung diseases. Here, we describe a primary adult human organoid model for investigating how inflammation shapes alveolar regeneration. Unlike previous models, this system supports long-term expansion of newly identified human-specific alveolar progenitor cells and serum-free differentiation into alveolar type 1 (AT1)-like cells. Using this platform, we find that interferon-gamma (IFN-γ) exerts cytotoxic effects on mature AT1-like cells while promoting survival of alveolar progenitor cells mediated by BIRC3. This unexpected selective positive effect of IFN-γ on alveolar progenitors underscores the need for nuanced and context-dependent evaluation of the influence of pro-inflammatory cytokines on alveolar regeneration. Our organoid model provides a reductionist platform for mechanistic studies and discovery of strategies to enhance alveolar regeneration.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The EMBO JournalPub Date : 2026-04-15DOI: 10.1038/s44318-026-00744-w
Khushdeep Bandesh,Efthymios Motakis,Siddhi Nargund,Romy Kursawe,Vijay Selvam, Ansarullah,Redwan M Bhuiyan,Giray Naim Eryilmaz,Amelia M Willett,Jacqueline K White,Sai Nivedita Krishnan,Cassandra N Spracklen,Duygu Ucar,Michael L Stitzel
{"title":"Deep single-cell decoding of human pancreatic islets reveals T2D β-cell gene expression defects.","authors":"Khushdeep Bandesh,Efthymios Motakis,Siddhi Nargund,Romy Kursawe,Vijay Selvam, Ansarullah,Redwan M Bhuiyan,Giray Naim Eryilmaz,Amelia M Willett,Jacqueline K White,Sai Nivedita Krishnan,Cassandra N Spracklen,Duygu Ucar,Michael L Stitzel","doi":"10.1038/s44318-026-00744-w","DOIUrl":"https://doi.org/10.1038/s44318-026-00744-w","url":null,"abstract":"Pancreatic islets maintain glucose homeostasis through coordinated action of endocrine and affiliate cell types and are central to type 2 diabetes (T2D) genetics and pathophysiology. Our understanding of robust human islet cell type-specific alterations in T2D remains limited. Here, we report comprehensive single-cell transcriptome profiling of 245,878 human islet cells from 48 donors spanning non-diabetic, pre-diabetic, and T2D states, and we identify 14 distinct cell types detected in every donor. Cell-cluster analysis reveals ~25-30% β-cell reductions consisting of β-cell loss and proportional increases in a senescent β-cell subpopulation in T2D donors, consistent with previous reports. Further, comparative data integration identifies 511 differentially expressed genes (DEGs) in T2D β-cells, including T2D-associated vitamin A metabolism genes, which are linked to impaired β-cell viability by multimodal functional validation. Integration with T2D genetic, proteomic, and mouse model metabolic phenotypes nominates 58 candidate causal T2D genes, including PDZK1 and GRAMD2B, which preserve β-cell mass. Together, this genomic resource provides an enhanced type 2 diabetes expression-atlas for data exploration, analysis, and hypothesis testing, as well as a novel genomic resource for insights into T2D pathophysiology and human islet dysfunction.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147684972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chromosomal instability promotes cell migration and invasion via EFEMP1 secretion into extracellular vesicles.","authors":"Siqi Zheng,Ruifang Tian,Marsudi Siburian,Anna Haider Rubio,Yuanyuan Liu,Rene Wardenaar,Marjan Shirzai,Laura Kempe,Emma Dijkstra,Eliza Warszawik,Maria Suarez Peredo Rodriguez,Klaas Sjollema,Petra L Bakker,Patrick van Rijn,Michaela Borghesan,Judith Tml Paridaen,Stefano Santaguida,Floris Foijer","doi":"10.1038/s44318-026-00766-4","DOIUrl":"https://doi.org/10.1038/s44318-026-00766-4","url":null,"abstract":"Triple-negative breast cancer (TNBC) is characterised by high rates of chromosomal instability (CIN) and rewired intercellular communication driven by both soluble factors and extracellular vesicles (EVs). To assess how CIN might affect EV-mediated signalling in TNBC, we studied the EV landscape of TNBC cell lines with induced CIN. We find that CIN leads to increased secretion of EVs and that these EVs promote cell migration of recipient cells. EVs are enriched for extracellular matrix (ECM) proteins, including EFEMP1. Indeed, modulation of EFEMP1 levels in EVs significantly alters migration behaviour of EV-treated cells. We show that EFEMP1 expression is regulated by STAT1, that EVs from STAT1-deficient cells no longer promote migration, and that this can be rescued by overexpression of EFEMP1 in STAT1-null cells. Xenografting TNBC cells with EFEMP1-enriched cells promotes migration in zebrafish embryos, suggesting that EFEMP1 expression is a factor that promotes metastasis. Together, our results identify a CIN-associated EV program in triple-negative breast cancer and highlight EFEMP1 as a potential therapeutic target to impair EV-driven tumour cell migration.","PeriodicalId":501009,"journal":{"name":"The EMBO Journal","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147666744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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