Experimental cell research最新文献

{"title":"Tsc1 and Tsc2 maintain hematopoietic homeostasis through multiple signaling pathways in Drosophila.","authors":"Zeming Wei, Haoyu Wang, Chenxu Zhai, Li Hua Jin, Shichao Yu","doi":"10.1016/j.yexcr.2026.115060","DOIUrl":"https://doi.org/10.1016/j.yexcr.2026.115060","url":null,"abstract":"<p><p>The lymph gland is the main hematopoietic tissue in Drosophila larvae, regulated by multiple signaling pathways and serving as a valuable genetic model for studying hematopoiesis. Investigating hematopoietic mechanisms in Drosophila can provide valuable insights into the pathogenesis of human hematopoietic malignancies. Tsc1 and Tsc2 are tumor suppressor genes mutated in tuberous sclerosis complex, a tumor syndrome. The protein complexes formed by their gene products have attracted considerable interest in the field of signaling research. However, their roles in maintaining hematopoietic homeostasis remain unclear. In this study, we found that knockdown of Tsc1 or Tsc2 in the intermediate zone and cortical zone leads to increased proliferation and differentiation of hemocytes, accompanied by disruption of progenitor cell maintenance in the medullary zone. Aberrant differentiation of lamellocytes was also observed, along with a marked increase in both the size and number of circulating hemocytes. Furthermore, Tsc1 or Tsc2 knockdown elevated levels of cell death in both the lymph gland and circulating hemocytes. Our findings suggest that Tsc1 and Tsc2 play multifaceted roles in regulating hematopoietic homeostasis through the TOR and Notch signaling pathways. Additionally, Tsc2 contributes to hematopoietic regulation via the JNK pathway and is also involved in apoptosis regulation. In conclusion, our findings revealed that Tsc1 and Tsc2 function within the intermediate zone and cortical zone of the lymph gland to maintain hematopoietic homeostasis through multiple signaling pathways.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115060"},"PeriodicalIF":3.5,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856159","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":"Atomic Force Microscopy Imaging of RBL-2H3 Cell Degranulation.","authors":"Jiani Li, Jing Hu, Yujuan Chen, Bowei Wang, Michael James Cardwell Crabbe, Zuobin Wang, Tuoyu Ju","doi":"10.1016/j.yexcr.2026.115059","DOIUrl":"https://doi.org/10.1016/j.yexcr.2026.115059","url":null,"abstract":"<p><p>Understanding the biophysical mechanisms of degranulation is crucial for managing allergic diseases, yet the spatiotemporal coordination of membrane and cytoskeletal dynamics during these reactions remains incompletely understood. In this study, we utilized Atomic Force Microscopy (AFM) to conduct a time-resolved investigation of RBL-2H3 cells during anti-DNP IgE-induced activation. By systematically mapping the cell surface, we quantified phase-specific changes in morphology, surface adhesion, and cortical stiffness (Young's modulus). Our results reveal a striking temporal asynchronicity, with cell height and surface adhesion peaking at 8 h, reflecting receptor-driven membrane ruffling and sensitization. In contrast, the Young's modulus reached its maximum at 12 h, indicating a delayed mechanical reinforcement driven by profound cytoskeletal rearrangement for active granule transport. Furthermore, we characterized the collapsed-sphere ultrastructure of secreted extracellular vesicles (EVs). These findings successfully decouple the initial membrane sensitization from the subsequent intracellular execution phase, identifying novel nanomechanical biomarkers to understand vesicle-mediated communication and to guide the design of stage-specific therapeutic interventions.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115059"},"PeriodicalIF":3.5,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835826","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 in vitro acquisition of CD11a by gastric cancer cells after contact with T cells via trogocytosis increases adhesion to endothelial cells.","authors":"Hideyo Miyato, Shin Saito, Hideyuki Ohzawa, Hironori Yamaguchi, Hiroshi Kawahira, Hisanaga Horie, Yoshinori Hosoya, Toshiki Mimura, Naohiro Sata, Joji Kitayama","doi":"10.1016/j.yexcr.2026.115028","DOIUrl":"https://doi.org/10.1016/j.yexcr.2026.115028","url":null,"abstract":"<p><strong>Background: </strong>Recent studies reveal that during trogocytosis plasma membranes are frequently transferred upon cell-to-cell contact, and that this phenomenon plays an important role in the modulation of anti-tumor immune response. However, the accompanying physiological roles in the tumor microenvironment are poorly understood.</p><p><strong>Methods & results: </strong>Human gastric cancer cell line OCUM-1 was co-cultured with T cells whose plasma membrane was stained with PKH26. Flow-cytometric analysis revealed that OCUM-1 was positive for PKH26 at one hour and the positive rate increased over time. The acquisition of PKH26 was dependent on cell-to-cell contact and suppressed when T cells were fixed. OCUM-1 came to express various immunological synapse molecules after 10 hours of co-culture (positive rate, CD45:73.6±7.9%, CD3: 35.5±10.1%, CD4: 15.3±14.7%, CD8: 7.7±2.4%, CD11a: 8.1±4.3%, CD11b: 3.4±1.9%). We focused on CD11a which belongs to β2 integrins and aids immune cell adherence to endothelial cells. After co-culture with activated T cells (LAK), the expression level of CD11a on OCUM-1 was accelerated (with T cells: 19.1±13.4%, with LAK: 75.2±11.8%) and the adhesion rate on endothelial cells increased in a CD11a dependent manner (adhesion rate, single-culture: 2.0±0.64%, co-culture: 6.3±2.0%, co-culture (pre-treat with CD11a antibody): 2.3±1.4%, n=10, single-culture vs co-culture, p<0.0001; co-culture vs pre-treat with CD11a antibody, p<0.0001).</p><p><strong>Conclusion: </strong>These results suggest that acquisition of CD11a from T cells by trogocytosis enables cancer cells to increase adhesive properties towards endothelial cells, which may result in intravenous metastasis promotion.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115028"},"PeriodicalIF":3.5,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835820","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":"CircRNA_38959 protects liver cells from intermittent hypoxia-triggered injury and suppresses ferroptosis by interacting with IGF2BP3.","authors":"Chaowei Li, Jinhuang Lin, Yanta Guo, Taiyong Fang, Yizhi Liang","doi":"10.1016/j.yexcr.2026.115047","DOIUrl":"10.1016/j.yexcr.2026.115047","url":null,"abstract":"<p><p>Intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), is closely associated with liver injury and ferroptosis. However, the molecular mechanisms underlying IH-induced liver damage remain largely unexplored. Here, we identify circ_38959 as a novel liver-protective circular RNA that mitigates IH-induced injury and ferroptosis. Circ_38959 overexpression in AML-12 hepatocytes significantly rescued cell viability, reduced apoptosis, and suppressed ferroptosis under IH conditions. Mechanistically, RNA immunoprecipitation uncovered that IGF2BP3 functions as a key interacting protein of circ_38959. Knocking down circ_38959 can down-regulate the protein expressions of IGF2BP3, c-Myc and c-Met. Functional studies revealed that IGF2BP3 deficiency abrogated the protective effects of circ_38959, confirming its essential role in liver protection and ferroptosis suppression. In an IH mouse model, AAV-mediated overexpression of circ_38959 effectively rescued liver function, and suppressed ferroptosis. Collectively, our study unveils a circ_38959-IGF2BP3 interaction that protects against IH-induced liver damage, highlighting circ_38959 as a potential therapeutic target for liver injury associated with OSA.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115047"},"PeriodicalIF":3.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812724","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":"Role of paraptosis in cancer: Molecular mechanisms and therapeutic potentials.","authors":"Yan-Ge Li, Meng-Yuan Hao, Hong-Jie Li, Hang-Shen Han, Umm E Laila, Wei-Rong Si, Qi-Ying Jiang, Dong-Dong Wu","doi":"10.1016/j.yexcr.2026.115050","DOIUrl":"10.1016/j.yexcr.2026.115050","url":null,"abstract":"<p><p>Paraptosis represents a mode of cell death, which is separate from classical apoptosis. Classical apoptotic pathways are caspase-dependent, accompanied by cell shrinkage, chromatin condensation, and apoptotic body formation. In contrast, paraptosis is characterized by cytoplasmic vacuolization without typical apoptotic nuclear alterations, and its signaling operates independently of the caspase system. Unlike apoptosis, paraptosis primarily depends on the mitogen-activated protein kinase (MAPK) signaling pathway for its mediation, highlighting its unique regulatory framework separate from classical apoptotic pathways. Since it does not overlap with apoptotic resistance mechanisms, inducing paraptosis holds great potential to overcome resistance to conventional chemotherapy and radiotherapy. Therefore, inducing paraptosis in cancer cells has crucial potential value for current cancer treatment. This article thoroughly explores the regulatory mechanisms of paraptosis and synthesizes its dual functions in the progression of cancer cells. Additionally, we discuss in detail cancer treatment strategies based on targeting paraptosis and analyze the feasibility and potential advantages of combining paraptosis with other cell death forms and various therapeutic methods to enhance cancer treatment efficacy.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115050"},"PeriodicalIF":3.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812846","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":"ALPK1 promotes cardiomyocyte hypertrophy by activating NF-κB/NLRP3 inflammasome-mediated pyroptosis.","authors":"Xiaomi Zhuang, Shuai Han, Zeyao Dong, Wenjie Pei, Jing Li, Haoxuan Sun, Mingyu Liu, Jing Lu","doi":"10.1016/j.yexcr.2026.115048","DOIUrl":"10.1016/j.yexcr.2026.115048","url":null,"abstract":"<p><strong>Background: </strong>Cardiac hypertrophy is a leading risk factor for cardiovascular morbidity and mortality. Alpha-protein kinase 1 (ALPK1) is a novel essential player in innate immunity and inflammation. Therapeutic agents targeting ALPK1 have successively entered clinical trials and become research hotspots. However, the role of ALPK1 on cardiac hypertrophy remains unknown.</p><p><strong>Methods: </strong>In the present study, transverse aortic constriction (TAC) was used to establish in vivo models of cardiac hypertrophy. Neonatal mouse cardiomyocytes (NMCMs) and AC16 human cardiomyocytes treated with angiotensin Ⅱ (Ang Ⅱ) were performed to mimic in vitro models of cardiac hypertrophy. ALPK1 gene expression was knocked down by small interfering RNAs (siRNAs) and overexpressed by transfection with plasmid, respectively.</p><p><strong>Results: </strong>ALPK1 was significantly upregulated in cardiac hypertrophy. ALPK1 knockdown effectively suppressed Ang Ⅱ-induced upregulated hypertrophic markers, enlarged cell surface area, decreased cell viability, increased lactate dehydrogenase release, enhanced caspase-1 activity, elevated positive pyroptotic cells, as well as the upregulation of p-NF-κB p65, NLRP3 inflammasome and pyroptosis markers in both NMCMs and AC16 cells. ALPK1 knockdown markedly suppressed the increased secretion of IL-1β and IL-18 induced by Ang Ⅱ in NMCMs. Consistently, ALPK1 over-expression significantly increased the expression of hypertrophic markers, enhanced the cell surface area, elevated the number of pyroptotic cells, upregulated the protein expression of NLRP3 inflammasome and pyroptosis markers, increased the secretion of IL-1β and IL-18, which were successfully reversed by the addition of MCC950, a selective NLRP3 inflammasome inhibitor. However, MCC950 treatment showed no effect on the upregulation of ALPK1 and p-NF-κB p65 induced by ALPK1 over-expression.</p><p><strong>Conclusion: </strong>ALPK1 promotes cardiomyocyte hypertrophy by activating NF-κB/NLRP3 inflammasome-mediated pyroptosis, providing new potential applications for agents targeting ALPK1 in the immunotherapy of cardiac hypertrophy.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115048"},"PeriodicalIF":3.5,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812731","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":"Matrix stiffness disrupts tight junction integrity in retinal pigment epithelial cells via YAP1-mediated autophagy suppression.","authors":"Songtao Wang, Yu Zhang, Ning Yang, Jinrong Cui, Jinsong Zhao","doi":"10.1016/j.yexcr.2026.115046","DOIUrl":"10.1016/j.yexcr.2026.115046","url":null,"abstract":"<p><strong>Background: </strong>The extracellular matrix (ECM) of retinal pigment epithelial (RPE) cells undergoes progressive stiffening during aging and under pathological conditions. However, how such mechanical effects affect RPE cell function remains incompletely understood. This study aims to investigate the effect of stiffness of ECM on autophagy in RPE cells and its regulatory role on tight junctions.</p><p><strong>Methods: </strong>ARPE-19 cells were cultured on polyacrylamide hydrogel substrates with low (5 kPa) and high (40 kPa) stiffness. The expression and subcellular localization of tight junction proteins and autophagy-related markers were assessed by Western blotting, quantitative PCR, and immunofluorescence staining. Autophagy was pharmacologically modulated using the autophagy activator rapamycin and the inhibitor chloroquine to evaluate the effects of autophagy on tight junction integrity. In addition, Yes-associated protein 1(YAP1) was knocked down using shRNA to investigate its role in ECM stiffness-mediated regulation of autophagy and tight junction alterations.</p><p><strong>Results: </strong>Polyacrylamide hydrogel substrates with low stiffness (5 kPa) and high stiffness (40 kPa) had no significant effect on the growth or proliferation of ARPE-19 cells. High-stiffness substrates markedly suppressed autophagic activity in ARPE-19 cells and downregulated the expression of tight junction proteins zonula occludens-1 (ZO-1), occludin, and claudin-19, resulting in disruption of tight junction integrity. Pharmacological inhibition of autophagy further exacerbated tight junction damage, whereas autophagy activation partially reversed the tight junction impairment induced by high matrix stiffness. Moreover, knockdown of YAP1 substantially attenuated the inhibitory effects of high stiffness on autophagy and tight junction protein expression.</p><p><strong>Conclusion: </strong>Increased ECM stiffness impairs tight junction integrity in ARPE-19 cells through a YAP1-mediated suppression of autophagy.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115046"},"PeriodicalIF":3.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766758","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":"Reinventing miRNA Cancer Therapy through Immunomodulation and AI.","authors":"Yue Zhou, Yiqiang Liu, Yuesheng Lv, Yan Fang, Chuan Xu, Hong Wu","doi":"10.1016/j.yexcr.2026.115041","DOIUrl":"https://doi.org/10.1016/j.yexcr.2026.115041","url":null,"abstract":"<p><p>Despite the rational therapeutic premise of microRNA (miRNA) replacement or inhibition for cancer treatment, its clinical translation remains significantly constrained. Major challenges span from inherent molecular instability and off-target effects to substantial delivery hurdles. This persistent translational impasse continues despite continuous advancements in oligonucleotide chemistry and delivery platform engineering, underscoring an urgent need to re-evaluate the current developmental pathway. This review systematically delineates the significant therapeutic potential of miRNAs as pivotal gene regulators in oncology, alongside the current challenges in clinical translation posed by their unique biological complexity and delivery hurdles. Considering that, we highlight two pivotal frontiers poised to reshape the field: first, the strategic integration of miRNA therapeutics with modern immunotherapies to enhance anti-tumor efficacy; second, the application of artificial intelligence (AI) to deconvolute miRNA biology and accelerate rational drug design. An objective appraisal of persistent translational barriers, including robust in vivo target validation, long-term safety, and the interpretability of complex computational models is also provided. We conclude that realizing the full clinical potential of miRNA therapy will necessitate a convergent approach, integrating intelligent delivery technologies, multi-omics-guided precision, and deep interdisciplinary collaboration.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115041"},"PeriodicalIF":3.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766763","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 ATF4/PSAT1/JNK Signaling Axis Suppresses Ferroptosis to Drive Venetoclax Resistance in AML.","authors":"XunXun Zhu, WenHui Huang, MingYan Zhang, YanLing Tao, Hao Zhang","doi":"10.1016/j.yexcr.2026.115045","DOIUrl":"https://doi.org/10.1016/j.yexcr.2026.115045","url":null,"abstract":"<p><p>Metabolic reprogramming has emerged as a key driver of therapy resistance in acute myeloid leukemia (AML). Here, we identify phosphoserine aminotransferase 1 (PSAT1) as a critical metabolic determinant of venetoclax (VEN) resistance through the suppression of ferroptosis. PSAT1 was consistently upregulated in VEN-resistant cell lines and relapsed patient samples. Mechanistically, the transcription factor ATF4 directly bound the PSAT1 promoter, enhancing its expression and subsequently promoting glutathione synthesis, depleting the labile iron pool, and attenuating lipid peroxidation. Concurrently, PSAT1 functioned to restrain JNK/c-Jun signaling. Knockdown of PSAT1 restored VEN sensitivity by triggering ferroptosis and modulating the expression of BCL-2 and GPX4. Clinically, elevated PSAT1 expression predicted poor patient survival. Our findings unveil the ATF4/PSAT1/JNK axis as a master regulator of ferroptosis in AML, revealing a druggable pathway to overcome VEN resistance.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115045"},"PeriodicalIF":3.5,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766807","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":"MDK promotes the mast cell activation and pancreatic fibrosis in mice with chronic pancreatitis via MDK-NCL signaling pathway.","authors":"Jianbin Xiong, Jian Song, Xing Jiang, Zhuanzhuan Huang, Yijie Zhang","doi":"10.1016/j.yexcr.2026.115043","DOIUrl":"10.1016/j.yexcr.2026.115043","url":null,"abstract":"<p><p>Chronic pancreatitis (CP) is characterized by persistent inflammation and fibrosis in the pancreas, but its exact pathogenesis remains unclear. To investigate the underlying mechanisms, human CP single-cell RNA sequencing (scRNA-seq) data (GSE208536) were analyzed for clustering and cell communication, while a dibutyltin dichloride (DBTC)-induced CP mouse model was established. Flow cytometry was used to analyze cell phenotypes and sort cells. Bioinformatics analysis revealed that pancreatic stellate cells (PSCs) and mast cells play a pivotal role in CP progression, with a significant enrichment in the midkine (MDK)-nucleolin (NCL) ligand-receptor pair. In CP mice, we confirmed concurrent upregulation of fibrotic markers (α-SMA, Collagen I, FN1) and mast cell mediators (HIS, MCT, NGF, C-kit, IL-18), alongside elevated MDK/NCL expression and infiltration of both PSCs and mast cells. Functional validation showed that MDK knockdown in PSCs reduced activation and fibrosis, and suppressed proliferation and degranulation in mast cells. These effects were reversed by recombinant MDK. Additionally, NCL neutralization blocked mast cell activation in wild-type co-cultures. Crucially, in vivo knockdown of MDK or NCL reduced cell infiltration and activation, thus alleviating pancreatic damage and fibrosis. In conclusion, the MDK-NCL axis contributes to interactions between PSCs and mast cells, thereby exacerbating fibrosis and inflammation in CP. These findings provide a mechanistic insight into CP pathogenesis and identify the MDK-NCL axis as a candidate for future functional studies.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"115043"},"PeriodicalIF":3.5,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766776","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}