European journal of cell biology最新文献

{"title":"Vimentin intermediate filaments facilitate transportation of hepatitis C virus components","authors":"Yifan Xing ,&nbsp;Shuzhi Cui ,&nbsp;Xinyi Huang ,&nbsp;Weisong Zhao ,&nbsp;Haoyu Li ,&nbsp;Jing Zhao ,&nbsp;Wakam Chang ,&nbsp;Shuangshuang Zhao ,&nbsp;Jin Zhong ,&nbsp;Yuxin Chen ,&nbsp;Yaming Jiu","doi":"10.1016/j.ejcb.2025.151505","DOIUrl":"10.1016/j.ejcb.2025.151505","url":null,"abstract":"<div><div>Vimentin, an intermediate filament protein, primarily contributes to intracellular organization, cell migration, and signal transduction. In recent years, the role of intermediate filaments in viral infection has garnered increasing attention. During viral infection, vimentin can regulate viral propagation by forming a vimentin cage to enclose viral replication factories, and facilitating the intracellular transport of viral components. However, whether vimentin can facilitate cell-to-cell transfer of viral components remains unknown. In this study, using hepatitis C virus (HCV) as a viral model, we demonstrated that HCV infection does not induce large-scale vimentin rearrangement or the formation of a vimentin cage. Interestingly, we observed that HCV components move directionally along a vimentin-containing cellular bridge from highly infected donor cells towards neighboring cells, potentially facilitating viral dissemination. Together, our findings unveil a previously unrecognized function of vimentin in the viral life cycle, expanding our understanding of the complex interplay between host cellular factors and viral strategies.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151505"},"PeriodicalIF":4.5,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144595599","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":"Cadmium exposure triggers vimentin phosphorylation via SIRT6-regulated AKT/PI3K signaling pathway in COPD","authors":"Rajesh Sinha ,&nbsp;Pooja Singh ,&nbsp;Huaxiu Zeng,&nbsp;Abhishek Kumar,&nbsp;Veena B. Antony","doi":"10.1016/j.ejcb.2025.151503","DOIUrl":"10.1016/j.ejcb.2025.151503","url":null,"abstract":"<div><div>Chronic Obstructive pulmonary disease (COPD) is a global health concern affecting over 300 million individuals worldwide, with airway fibrosis and subsequent small airway narrowing identified as the primary mechanism driving disease progression. This pathological process is characterized by accelerating lung aging, manifesting as reduced cellular growth and increased expression of cyclin-dependent kinase inhibitors in fibroblasts, which we have demonstrated in our previous study utilizing a cadmium-induced COPD mouse model. Cadmium, a toxic heavy metal, penetrates deep into the lung airways inducing oxidative stress, promoting extracellular matrix deposition, and triggering inflammatory reactions. The present study elucidates that cadmium exposure results in the inhibition of sirtuin-6 (SIRT6) which promotes phosphorylation of the AKT/PI3K signaling pathway, which in turn leads to phosphorylation of vimentin, an intermediate filament protein. Cadmium increases extracellular vimentin which is phosphorylated through AKT/PI3K signaling due to SIRT6 inhibition. Vimentin inhibition using siRNA transfection study suggested no effect on SIRT6, phosphorylated AKT and PI3K expression. SIRT6 induction (UBCS039) in fibroblasts leads to a decrease in phosphorylated AKT/PI3K inhibiting extracellular vimentin levels (P = 0.0002) in cadmium-exposed cells. The present work proposes role of SIRT6 in regulation of vimentin, an important intermediate filament in pathogenesis of COPD.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151503"},"PeriodicalIF":4.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144523471","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":"Integrated phenotypic and transcriptomic characterization of desmin-related cardiomyopathy in hiPSC-derived cardiomyocytes and machine learning-based classification of disease features","authors":"Vivien Batoumeni ,&nbsp;Yeranuhi Hovhannisyan ,&nbsp;Bénédicte Gobert ,&nbsp;Keyhan Alvandipour ,&nbsp;Jennifer Arthur Ataam ,&nbsp;Ombline Conrad ,&nbsp;David Hoffmann ,&nbsp;Nicolas Wiest-Daesslé ,&nbsp;Jochen Dobner ,&nbsp;José Américo Nabuco Leva Ferreira Freitas ,&nbsp;Hakim Hocini ,&nbsp;Zhenlin Li ,&nbsp;Laurent Brino ,&nbsp;Andrea Rossi ,&nbsp;Onnik Agbulut ,&nbsp;Peter Sommer ,&nbsp;Pierre Joanne ,&nbsp;Konstantinos Gkatzis","doi":"10.1016/j.ejcb.2025.151502","DOIUrl":"10.1016/j.ejcb.2025.151502","url":null,"abstract":"<div><div>Desmin-related diseases are characterized by skeletal muscle weakness, cardiomyopathy, and respiratory dysfunction due to mutations in the desmin gene (<em>DES</em>), which encodes a protein essential for muscle cell integrity. This study investigates the effects of a pathogenic desmin mutation (<em>DES</em>^E439K) in human cardiomyocytes derived from human induced pluripotent stem cells (hiPSCs) obtained from a patient carrying the <em>DES</em>^E439K mutation, compared to cardiomyocytes derived from hiPSCs of three healthy donors. To further validate our findings a genome edited cell line has been obtained following the insertion of the mutation in a control hiPSC line. Using advanced technologies, including transcriptomics and phenotypic machine learning algorithms, we analyzed how this mutation disrupts cellular function and contributes to disease phenotypes. Our findings reveal that cardiomyocytes carrying <em>DES</em>^E439K exhibit cytoplasmic protein aggregation, mitochondrial and sarcomere defects, and contractile dysfunctions, highlighting key phenotypic defects in desmin-related cardiomyopathy. Finaly, we developed a machine learning prediction model to classify cellular phenotypes, which can be used for translational research, including drug candidate screening. This research opens new avenues for understanding the molecular mechanisms of desmin-related cardiomyopathies and fosters the development of novel therapeutic strategies.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151502"},"PeriodicalIF":4.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579897","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":"Ropivacaine and lidocaine inhibit SaOS-2 osteosarcoma cell proliferation and invasion via mitochondrial dysfunction and apoptosis","authors":"Inna Zumberg,&nbsp;Amir Hashemi,&nbsp;Masoumeh Ezati,&nbsp;Larisa Chmelikova,&nbsp;Katerina Ingrova,&nbsp;Vratislav Cmiel","doi":"10.1016/j.ejcb.2025.151501","DOIUrl":"10.1016/j.ejcb.2025.151501","url":null,"abstract":"<div><div>Local anesthetics are routinely used for pain management, yet their broader effects on cancer cells remain incompletely understood. Here, we investigate the impact of ropivacaine hydrochloride and lidocaine hydrochloride monohydrate on SaOS-2 human osteosarcoma cells using a series of <em>in vitro</em> assays. Our findings indicate that both anesthetics markedly reduce cell viability and proliferation, as measured by XTT and Colony formation assays, respectively. Mechanistic studies reveal significant disruption of mitochondrial function, evidenced by decreased membrane potential, enhanced mitochondrial superoxide production, and pronounced mitochondrial fragmentation. Concurrently, the expression of matrix metalloproteinases (MMP-2 and MMP-9) is downregulated, while pro-apoptotic markers (Caspase-3, Caspase-9, and BAX) are upregulated. Neither agent alters Vimentin or E-cadherin expression, suggesting a limited effect on epithelial-mesenchymal transition pathways. Notably, lidocaine and ropivacaine also inhibit SaOS-2 cell migration and invasion, as demonstrated by Scratch, single-cell migration, and Transwell invasion assays. Furthermore, both agents suppress alkaline phosphatase activity, a hallmark associated with osteosarcoma differentiation and metastatic potential. Taken together, these results support the conclusion that ropivacaine and lidocaine exert broad anti-tumor effects by impairing both mitochondrial homeostasis and the invasive phenotype in osteosarcoma cells. Their capacity to mitigate core hallmarks of malignancy underscores the need for further investigation into local anesthetics as potential adjuvant therapies for osteosarcoma.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151501"},"PeriodicalIF":4.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501110","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":"Genetic compensation highlights the importance of neural cell adhesion molecule Ncam1 paralogs in balancing signaling pathways during zebrafish lateral line development","authors":"Annemarie Lange,&nbsp;Martin Bastmeyer,&nbsp;Joachim Bentrop","doi":"10.1016/j.ejcb.2025.151500","DOIUrl":"10.1016/j.ejcb.2025.151500","url":null,"abstract":"<div><div>The neural cell adhesion molecule NCAM1 is essential for neuronal development and enables organized cell migration, axon growth, and fasciculation. As a result of genome duplication in zebrafish, the paralogs Ncam1a and Ncam1b arose. Our previously published findings using morpholino knockdown experiments demonstrated the essential role of Ncam1b in the development of the zebrafish lateral line system, a mechanosensory organ critical for detecting water movements. <em>ncam1b</em> morphants exhibited severe defects, including impaired primordium migration, disrupted proneuromast deposition, and reduced cell proliferation within the primordium. These defects were linked to a disrupted interaction between Ncam1b and Fgfr1a, which led to compromised proliferation and abnormal lateral line development. The current study reveals that <em>ncam1b</em> mutants, however, unlike morphants, do not show this severe phenotype. Instead, we observed subtle alterations, including altered FGF and Wnt signaling and a redistribution of proliferating cells within the primordium. Notably, <em>ncam1b</em> mutants displayed elevated levels of the paralog <em>ncam1a</em> mRNA. The knockdown of either <em>ncam1a</em> or <em>upf3a</em> in <em>ncam1b</em> mutants resulted in a phenotype resembling that of <em>ncam1b</em> morphants. Upf3a is a key regulator of genetic compensation, a well-known phenomenon in zebrafish research. This supports the hypothesis that upregulated <em>ncam1a</em> compensates for the loss of <em>ncam1b</em>, facilitating normal lateral line development. These findings emphasize the essential role of Ncam1 in zebrafish lateral line development and suggest that the retention of both paralogs, <em>ncam1a</em> and <em>ncam1b</em>, acts as a protective mechanism to ensure the preservation of critical Ncam1 functions after gene duplication.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151500"},"PeriodicalIF":4.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471038","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":"Editorial - Advances in cell, tissue, organ engineering, and organoid technology.","authors":"Shoen Kume, Yoichi Tagawa, Ryuichi Okamoto, Hiroshi Kawasaki","doi":"10.1016/j.ejcb.2025.151499","DOIUrl":"https://doi.org/10.1016/j.ejcb.2025.151499","url":null,"abstract":"","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":" ","pages":"151499"},"PeriodicalIF":4.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316187","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":"Considerations for developing CYP induction assays in hepatocytes: Insights from a multilaboratory study","authors":"Hiroko Toyoda ,&nbsp;Ayaka Nozue ,&nbsp;Yuki Nishida ,&nbsp;Yasuko Yakabe ,&nbsp;Yasuhiko Aiki ,&nbsp;Yukiko Ueyama-Toba ,&nbsp;Kazuo Takayama ,&nbsp;Hiroyuki Mizuguchi ,&nbsp;Chihiro Mori ,&nbsp;Yu-suke Torisawa ,&nbsp;Yoko Sakai ,&nbsp;Takahiro Iwao ,&nbsp;Tamihide Matsunaga ,&nbsp;Shinichiro Horiuchi ,&nbsp;Daiju Yamazaki ,&nbsp;Seiichi Ishida ,&nbsp;Nobuhiko Kojima ,&nbsp;Kosuke Inamura ,&nbsp;Yasuyuki Sakai ,&nbsp;Masaki Nishikawa ,&nbsp;Yuzuru Ito","doi":"10.1016/j.ejcb.2025.151497","DOIUrl":"10.1016/j.ejcb.2025.151497","url":null,"abstract":"<div><div>Cytochrome P450 (CYP) induction studies using primary human hepatocytes (PHH) were conducted across seven laboratories. Standard operating procedures (SOPs) were developed and distributed, ensuring all laboratories used PHH from the same donor and CYP inducers prepared at a single location. In each laboratory, PHH was seeded, cultured, and tested for CYP induction. Induction levels of CYP1A2, CYP2B6, and CYP3A4 mRNA were analyzed by collecting and processing PHH lysates at one site. A review of laboratory work records revealed differences in PHH seeding density and CYP inducer treatment times, which were suggested as potential sources of variability in RNA yield and CYP induction patterns. Follow-up tests confirmed that both seeding density and induction duration significantly influenced CYP mRNA expression levels, beyond lot-to-lot differences in PHH. Despite adhering to shared SOPs, these inconsistencies contributed to variability in study results. To address these challenges, we discuss key considerations for SOP development and implementation to improve reproducibility in CYP induction assays.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151497"},"PeriodicalIF":4.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306430","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":"Self-organization and applications of neural organoids","authors":"Hideya Sakaguchi","doi":"10.1016/j.ejcb.2025.151496","DOIUrl":"10.1016/j.ejcb.2025.151496","url":null,"abstract":"<div><div>Organoid technology has become a field that attract many researcher’s attention and involvement. “Organoid” is a coined word which means organ like-tissue (Organ+oid), and organoid is determined as stem cell-derived three-dimensional (3D) tissues that recapitulate developmental processes and tissue specific function in vivo. Generally, they are derived from pluripotent stem cells (PSCs) including induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs), or from tissue stem cells. The first report that created human 3D cerebral tissue arose in 2008 which is currently considered as the pioneering work of “neural organoid” (Eiraku et al., 2008, Sasai 2013a, Sasai 2013b). The neural organoids provide living human neural tissues that bring opportunities to study human development, human neuroscience, neurological and psychiatric disorders, and evolutions. The neural organoid can be said as “cut &amp; paste” of developmental biological process into a dish. Thus, understanding the background of neural organoid needs developmental knowledge, but current organoid researches looks to use organoid as a tool to study the aim that the researchers want to focus. This leads the organoid research more methodological, and the improvement or sophistication of organoid methods has still been difficult for most of new coming researchers. For this problem, this review provide insights of how to assemble organoid methods from viewpoints of development especially from morphological/structual changes. In this review, I start from the brief history of how neural organoid research emerged from developmental biology. Then I introduce some interesting aspects of neural organoid generation focusing on self-organization of regions and structures. From the viewpoint of a developer of this field, this review also show how to think and adjust the methods to generate novel regional organoids taking hippocampal organoids as an example. Regarding structural self-organization I will introduce cerebral organoid for an example of layer organization in a dish. By showing background knowledge with scientific achievements and interesting aspects, this review will help researchers who want to create novel neural organoids.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151496"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185230","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":"Tri-culture model of intestinal epithelial cell, macrophage, and bacteria for the triggering of inflammatory bowel disease on a microfluidic device","authors":"Shiori Tamura ,&nbsp;Clarissa Ellice Talitha Pasang ,&nbsp;Minami Tsuda ,&nbsp;Shilan Ma ,&nbsp;Hiromasa Shindo ,&nbsp;Noriyuki Nagaoka ,&nbsp;Tomoki Ohkubo ,&nbsp;Yoichi Fujiyama ,&nbsp;Miho Tamai ,&nbsp;Yoh-ichi Tagawa","doi":"10.1016/j.ejcb.2025.151495","DOIUrl":"10.1016/j.ejcb.2025.151495","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) involves gastrointestinal inflammation, due to intestinal epithelial barrier destruction caused by excessive immune activation. Conventional cell culture systems do not provide a model system that can recapitulate the complex interactions between epithelial cells, immune cells, and intestinal bacteria. To address this, we developed a microfluidic device that mimics the inflammatory response associated with microbial invasion of the intestinal mucosa. The device consisted of two media channels, an upper and a lower channel, and a porous membrane between these channels on which C2BBe1 intestinal epithelial cells were seeded to form a tight junction layer. Each electrode was placed in contact with both channels to continuously monitor the tight junction state. Fresh medium flow allowed bacterial numbers to be controlled and bacterial toxins to be removed, allowing co-culture of mammalian cells and bacteria. In addition, RAW264 macrophage cells were attached to the bottom of the lower channel. By introducing <em>E. coli</em> into the lower channel, the RAW264 cells were activated and produced TNF-α, successfully recapitulating a culture model of inflammation in which the C2BBe1cell tight junction layer was destroyed. The main structure of the device was initially made of polydimethylsiloxane to facilitate its widespread use, but with a view to introducing anaerobic bacteria in the future, a similar phenomenon was successfully reproduced using polystyrene. When TPCA-1, an IκB kinase 2 inhibitor was added into this IBD culture model, the tight junction destruction was significantly suppressed. The results suggest that this IBD culture model also is useful as a screening system for anti-IBD drugs.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151495"},"PeriodicalIF":4.5,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144117049","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":"microRNA-183–5p induces cell density-dependent apoptosis through the regulation of Presenilin 2","authors":"Yuki Yabuuchi ,&nbsp;Yosuke Matsuno ,&nbsp;Kai Yazaki ,&nbsp;Wei Zhen Ting ,&nbsp;Kengo Nishino ,&nbsp;Sosuke Matsumura ,&nbsp;Kenya Kuramoto ,&nbsp;Kazufumi Yoshida ,&nbsp;Masashi Matsuyama ,&nbsp;Takumi Kiwaoto ,&nbsp;Yuko Morishima ,&nbsp;Nobuyuki Hizawa","doi":"10.1016/j.ejcb.2025.151494","DOIUrl":"10.1016/j.ejcb.2025.151494","url":null,"abstract":"<div><div>Cells undergo apoptosis under dense culture condition to maintain homeostasis. Impaired apoptosis may contribute to the excessive accumulation of pathogenetic cells in such diseases as cancer and organ fibrosis. Elucidating the molecular mechanisms regulating cell density-dependent apoptosis may provide novel therapeutic strategy against these diseases. We have reported Notch signaling, activated by γ-secretase under dense culture condition, regulates cell density-dependent apoptosis through the induction of IL-6. Presenilin 2 (PSEN2) is a subunit of γ-secretase and has been shown to modulate apoptosis. The role for PSEN2 in cell density-dependent apoptosis and Notch signaling activation, however, remains unclear. Here, we show a crucial role for PSEN2 in the regulation of cell density-dependent apoptosis in NIH 3T3 cells. PSEN2 protein primarily existed as C-terminal fragment (CTF). PSEN2 CTF expression was upregulated as cell density increased. PSEN2 regulated the development of apoptosis, which is accompanied by increased Bcl-2 expression, decreased Bax expression, and activated PI3K/Akt pathway. PSEN2 is predicted to be targeted by microRNA-183–5p (miR-183–5p) by several algorithms. We verified miR-183–5p directly regulates PSEN2 expression and induces apoptosis. In conclusion, our results demonstrate a crucial role of PSEN2 and its regulation by miR-183–5p in the regulation of cell density-dependent apoptosis.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151494"},"PeriodicalIF":4.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941191","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}