Cell Death and Differentiation最新文献

{"title":"Alternative spliceosomal protein Eftud2 mediated Kif3a exon skipping promotes SHH-subgroup medulloblastoma progression","authors":"Ying Li, Liping Chen, Saisai Xue, Zhihong Song, Heli Liu, Hao Li, Wei Shen, Chen Zhang, Haitao Wu","doi":"10.1038/s41418-025-01512-9","DOIUrl":"https://doi.org/10.1038/s41418-025-01512-9","url":null,"abstract":"<p>Alternative splicing plays a pivotal role in various facets of organogenesis, immune response, and tumorigenesis. Medulloblastoma represents a prevalent childhood brain tumor, with approximately one-third classified as the Sonic Hedgehog (SHH) subgroup. Nevertheless, the contribution of alternative splicing to medulloblastoma oncogenesis remains elusive. This investigation delineated an upregulation of the spliceosomal protein Eftud2 in the SHH-subgroup medulloblastoma mouse model and human medulloblastoma patients. Targeted ablation of <i>Eftud2</i> in granule precursor cells (GNPs) within the cerebellum prolonged the survival of SHH-subgroup medulloblastoma mice, indicating a putative association between Eftud2 expression and medulloblastoma prognosis. Functional assays unveiled that <i>EFTUD2</i> depletion in human medulloblastoma cells significantly curtailed cellular proliferation by impeding the activation of the SHH signaling pathway. Through multi-omics sequencing analysis, it was discerned that Eftud2 influences exons 10–11 skipping of <i>Kif3a</i>, a kinesin motor critical for primary cilia formation. Notably, exons 10–11 skipping in <i>Kif3a</i> augmented human medulloblastoma cell proliferation by potentiating the transcriptional activity of Gli2. These findings underscore a robust correlation between Eftud2 and SHH-subgroup medulloblastoma, emphasizing its regulatory role in modulating downstream transcription factors through the alternative splicing of pivotal genes within the SHH signaling pathway, thereby propelling the aggressive proliferation of SHH-subgroup medulloblastoma.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"261 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TTK promotes mitophagy by regulating ULK1 phosphorylation and pre-mRNA splicing to inhibit mitochondrial apoptosis in bladder cancer","authors":"Kang Chen, Jinyu Chen, Yukun Cong, Qingliu He, Chunyu Liu, Jiawei Chen, Haoran Li, Yunjie Ju, Liang Chen, Yarong Song, Yifei Xing","doi":"10.1038/s41418-025-01492-w","DOIUrl":"https://doi.org/10.1038/s41418-025-01492-w","url":null,"abstract":"<p>Bladder cancer (BC) remains a major global health challenge, with poor prognosis and limited therapeutic options in advanced stages. TTK protein kinase (TTK), a serine/threonine kinase, has been implicated in the progression of various cancers, but its role in BC has not been fully elucidated. In this study, we show that TTK is significantly upregulated in BC tissues and cell lines, correlating with poor patient prognosis. Functional assays revealed that TTK promotes proliferation and inhibits apoptosis of BC cells. Mechanistically, TTK enhances mitophagy by directly phosphorylating ULK1 at Ser477, thereby activating the ULK1/FUNDC1-mediated mitophagy pathway. TTK knockdown disrupts mitophagy, leading to impaired clearance of damaged mitochondria, excessive accumulation of mitochondrial reactive oxygen species (mtROS), and activation of mitochondrial apoptosis. Furthermore, TTK phosphorylates SRSF3 at Ser108, preventing ULK1 exon 5 skipping and maintaining ULK1 mRNA stability. These findings show that TTK plays a key role in maintaining mitophagy in BC cells. Targeting TTK could offer a promising new approach for BC treatment by disrupting mitophagy and inducing mitochondrial apoptosis.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"46 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combinatorial tagging generates a multi-purpose knock-in mouse model revealing phase separation-dependent germ granules in RNA homeostasis and germline development","authors":"Lan Meng, Caoling Xu, Yuzhu Cao, Limin Wu, Yuzhang Zhu, Jiaqi Zou, Islam Uddin, Iqra Zafar, Azhar Muhammad, Xuemei Xing, Ren-tao Jin, Li He, Hongbin Liu, Wenqing Li, Jianqiang Bao","doi":"10.1038/s41418-025-01495-7","DOIUrl":"https://doi.org/10.1038/s41418-025-01495-7","url":null,"abstract":"<p>A large resource of epitope-tagged and Cre/CreERT2-expressing mouse models are available for studying germ granules and germline development. Germ granules are proteinaceous, membraneless organelles (MLO) involved in germ cell differentiation and maturation; however, their protein and RNA transcript constituents, as well as their functional mechanisms remain incompletely understood. Herein, we generated a versatile germline mouse model through combinatorially tagging DDX4 to enable simultaneous expression of three cistronic coding products (C-terminally tagged DDX4 - DDX4^5HA, EGFP, and CreERT2) under the control of the endogenous <i>Ddx4</i> promoter. By leveraging the high-affinity HA tag, we optimized an efficient workflow to purify germ granules (Chromatoid body, CB) from spermatids, and characterized their protein and RNA transcript composition. Moreover, we explored and ascertained that DDX4-mediated, phase-separation dependent CB integrity is functionally important for recruiting distinctive long RNA transcripts and for the biogenesis of pachytene- and TE-derived piRNAs. Together, our study generated a versatile germline mouse model with a multiplicity of applications for germline study, and provided mechanistic insights into germline development as dictated by germ granules.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative multiomic approaches reveal ZMAT3 and p21 as conserved hubs in the p53 tumor suppression network","authors":"Anthony M. Boutelle, Aicha R. Mabene, David Yao, Haiqing Xu, Mengxiong Wang, Yuning J. Tang, Steven S. Lopez, Sauradeep Sinha, Janos Demeter, Ran Cheng, Brooks A. Benard, Edel M. McCrea, Liz J. Valente, Alexandros P. Drainas, Martin Fischer, Ravindra Majeti, Dmitri A. Petrov, Peter K. Jackson, Fan Yang, Monte M. Winslow, Michael C. Bassik, Laura D. Attardi","doi":"10.1038/s41418-025-01513-8","DOIUrl":"https://doi.org/10.1038/s41418-025-01513-8","url":null,"abstract":"<p><i>TP53</i>, the most frequently mutated gene in human cancer, encodes a transcriptional activator that induces myriad downstream target genes. Despite the importance of p53 in tumor suppression, the specific p53 target genes important for tumor suppression remain unclear. Recent studies have identified the p53-inducible gene <i>Zmat3</i> as a critical effector of tumor suppression, but many questions remain regarding its p53-dependence, activity across contexts, and mechanism of tumor suppression alone and in cooperation with other p53-inducible genes. To address these questions, we used Tuba-seq^Ultra somatic genome editing and tumor barcoding in a mouse lung adenocarcinoma model, combinatorial in vivo CRISPR/Cas9 screens, meta-analyses of gene expression and Cancer Dependency Map data, and integrative RNA-sequencing and shotgun proteomic analyses. We established <i>Zmat3</i> as a core component of p53-mediated tumor suppression and identified <i>Cdkn1a</i> as the most potent cooperating p53-induced gene in tumor suppression. We discovered that ZMAT3/CDKN1A serve as near-universal effectors of p53-mediated tumor suppression that regulate cell division, migration, and extracellular matrix organization. Accordingly, combined <i>Zmat3</i>-<i>Cdkn1a</i> inactivation dramatically enhanced cell proliferation and migration compared to controls, akin to <i>p53</i> inactivation. Together, our findings place <i>ZMAT3</i> and <i>CDKN1A</i> as hubs of a p53-induced gene program that opposes tumorigenesis across various cellular and genetic contexts.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"5 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-associated reduction in ER-Mitochondrial contacts impairs mitochondrial lipid metabolism and autophagosome formation in the heart","authors":"Weilong Hong, Xue Zeng, Ruiyan Ma, Yu Tian, Huimin Miu, Xiaoping Ran, Rui Song, Zhenchun Luo, Dapeng Ju, Daqing Ma, Milad Ashrafizadeh, Sujit Kumar Bhutia, João Conde, Gautam Sethi, He Huang, Chenyang Duan","doi":"10.1038/s41418-025-01511-w","DOIUrl":"https://doi.org/10.1038/s41418-025-01511-w","url":null,"abstract":"<p>The accumulation of dysfunctional giant mitochondria is a hallmark of aged cardiomyocytes. This study investigated the core mechanism underlying this phenomenon, focusing on the disruption of mitochondrial lipid metabolism and its effects on mitochondrial dynamics and autophagy, using both naturally aging mouse models and etoposide-induced cellular senescence models. In aged cardiomyocytes, a reduction in endoplasmic reticulum-mitochondrial (ER-Mito) contacts impairs lipid transport and leads to insufficient synthesis of mitochondrial phosphatidylethanolamine (PE). A deficiency in phosphatidylserine decarboxylase (PISD) further hinders the conversion of phosphatidylserine to PE within mitochondria, exacerbating the deficit of PE production. This PE shortage disrupts autophagosomal membrane formation, leading to impaired autophagic flux and the accumulation of damaged mitochondria. Modulating LACTB expression to enhance PISD activity and PE production helps maintain mitochondrial homeostasis and the integrity of aging cardiomyocytes. These findings highlight the disruption of mitochondrial lipid metabolism as a central mechanism driving the accumulation of dysfunctional giant mitochondria in aged cardiomyocytes and suggest that inhibiting LACTB expression could serve as a potential therapeutic strategy for mitigating cardiac aging and preserving mitochondrial function.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"1 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143851005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DUBA sustains the stability of NOD2 and RIPK2 to enhance innate immune responses","authors":"Bincheng Zhou, Maojin Yin, Xian Su, Suhui Sheng, Xue Du, Jiangyun Shen, Kangmin Chen, Deqi Wang, Zhenhu Zhu, Yanqi Xu, Zhongding Li, Jianmin Li, Yuhua Li, Jing Ruan, Xu Wang","doi":"10.1038/s41418-025-01516-5","DOIUrl":"https://doi.org/10.1038/s41418-025-01516-5","url":null,"abstract":"<p>Nucleotide-binding oligomerization domain containing 2 (NOD2) detects conserved fragments of bacterial peptidoglycan in the cytosol and induces innate immune responses. Here, we found that the NOD2 signaling pathway was critically regulated by the deubiquitinating enzyme DUBA. DUBA-deficient macrophages were defective in NOD2 signaling and produced significantly lower amounts of cytokines and chemokines in response to muramyl dipeptide (MDP). DUBA potentiated NOD2-mediated signal transduction by maintaining the protein levels of NOD2 and receptor-interacting protein kinase 2 (RIPK2). Mechanistically, DUBA interacted with NOD2 and RIPK2 and removed K48-linked polyubiquitin chains from them through enzymatic activity, thereby inhibiting the proteasomal degradation of NOD2 and RIPK2. Macrophage-specific ablation of DUBA attenuated MDP-induced systematic inflammation and liver injury in mice. In addition, DUBA deficiency in macrophages rendered mice hypersensitive to DSS-induced colitis and eliminated the protective effect of MDP treatment in colitis. Thus, DUBA acts as an important regulator of NOD2-mediated signaling and innate immune responses.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"41 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD95/Fas stoichiometry in future precision medicine","authors":"Mauricio Sica, Murielle Roussel, Patrick Legembre","doi":"10.1038/s41418-025-01493-9","DOIUrl":"https://doi.org/10.1038/s41418-025-01493-9","url":null,"abstract":"<p>CD95, also known as Fas, belongs to the tumor necrosis factor (TNF) receptor superfamily. The main biological function of this receptor is to orchestrate and control the immune response since mutations in CD95 or deregulation of its downstream signaling pathways lead to auto-immunity and inflammation. Interestingly, more than twenty years ago, pioneer studies highlighted that like TNFR1, TRAILR1 or CD40, CD95 pre-associates at the plasma membrane in a ligand-independent fashion. This self-association occurs through a domain designated pre-ligand assembly domain or PLAD. Although the disruption of this pre-association prevents CD95 signaling, no drugs targeting this region have been generated because many questions remain on the stoichiometry and conformation of this receptor. Despite more than 40.000 publications, no crystal structure of CD95 alone or in combination with its ligand, CD95L, exists. Based on other TNFR members, we herein discuss the predicted conformation of CD95 at the plasma membrane and how these putative structures might account for the induction of the cell signaling pathways.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"17 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel role of exostosin glycosyltransferase 2 (EXT2) in glioblastoma cell metabolism, radiosensitivity and ferroptosis","authors":"Rocío Matesanz-Sánchez, Mirko Peitzsch, Inga Lange, Jovan Mircetic, Michael Seifert, Nils Cordes, Anne Vehlow","doi":"10.1038/s41418-025-01503-w","DOIUrl":"https://doi.org/10.1038/s41418-025-01503-w","url":null,"abstract":"<p>Glioblastoma (GBM) employs various strategies to resist therapy, resulting in poor patient survival. A key aspect of its survival mechanisms lies in metabolic regulation, maintaining rapid growth and evading cell death. Recent studies revealed the connection between therapy resistance and ferroptosis, a lipid peroxidation-dependent cell death mechanism triggered by metabolic dysfunction. Our aim was to identify novel regulators of therapy resistance in GBM cells. We conducted a comprehensive analysis combining RNA-sequencing data from a panel of human GBM cell models and TCGA GBM patient datasets. We focused on the top-12 differentially expressed gene candidates associated with poor survival in GBM patients and performed an RNA interference-mediated screen to uncover the radiochemosensitizing potential of these molecules and their impact on metabolic activity, DNA damage, autophagy, and apoptosis. We identified exostosin glycosyltransferase 2 (EXT2), an enzyme previously described in heparan sulfate biosynthesis, as the most promising candidate. EXT2 depletion elicited reduced cell viability and proliferation as well as radiochemosensitization in various GBM cell models. Mechanistically, we explored EXT2 function by conducting untargeted and targeted metabolomics and detected that EXT2-depleted GBM cells exhibit a differential abundance of metabolites belonging to S-adenosylmethionine (SAM) metabolism. Considering these metabolic changes, we determined lipid peroxidation and found that the diminished antioxidant capacity resulting from decreased levels of metabolites in the transsulfuration pathway induces ferroptosis. Moreover, modifications of specific SAM and transsulfuration metabolism associated enzymes revealed a prosurvival and ferroptosis-reducing function when EXT2 is depleted. Collectively, our results uncover a novel role of EXT2 in GBM cell survival and response to X-ray radiation, which is controlled by modulation of ferroptosis. These findings expand our understanding of how GBM cells respond to radio(chemo)therapy and may contribute to the development of new therapeutic approaches.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"95 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the poliovirus receptor to activate T cells and induce myeloid-derived suppressor cells to differentiate to pro-inflammatory macrophages via the IFN-γ-p-STAT1-IRF8 axis in cancer therapy","authors":"Mingyang Feng, Qizhi Ma, Benxia Zhang, Yue Chen, Yang Yang, Xia He, Yao Zeng, Meng Jing, Xuejin Ou, Yixian Liu, Qian Li, Weiting Liao, Xiaoyu Li, Sirui Tan, Diyuan Qin, Dan Li, Qiu Li, Yongsheng Wang","doi":"10.1038/s41418-025-01496-6","DOIUrl":"https://doi.org/10.1038/s41418-025-01496-6","url":null,"abstract":"<p>T cell immunoglobulin and ITIM domain (TIGIT) is one of the most important immune checkpoints expressed on lymphocytes, and poliovirus receptor (PVR, also CD155) serves as the most crucial ligand for TIGIT, harboring an important function in cancer cells and influencing the tumor microenvironment (TME). While it’s well-established that TIGIT blockade could reverse immunosuppression, the question of whether direct inhibition of PVR yields comparable results remains to be fully elucidated. This study investigated the role of PVR within the TME on the LLC, CT26 and MC38 tumor models and found that direct blockade of PVR on tumor cells could trigger T cell activation, enhance the production of immunostimulatory cytokine IFN-γ, and drive the differentiation of intratumoral myeloid-derived suppressor cells (MDSCs) into pro-inflammatory macrophages through the IFN-γ-p-STAT1-IRF8 axis. Furthermore, this study found that the anti-PVR nanobody monotherapy reduced tumor volume in the CT26 and MC38 tumor models. Combination of anti-PVR nanobody and anti-PD-1 antibody was effective in the LLC, CT26 and MC38 tumor models and had acceptable toxicity. These findings collectively suggest that PVR exhibits considerable promise as a therapeutic target in the development of immunotherapies aimed at augmenting the anti-tumor immune response.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"108 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143827666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycogen stores mediated by the p53-GYS1 feedback circuit engenders platinum resistance in ovarian clear cell carcinoma","authors":"Hao-Yu Liang, Rong-Zhen Luo, Ru Deng, Shi-Lu Chen, Xuan Liu, Xia Yang, Li-Jun Wei, Zong-Qiang Wei, Li-Yan Wu, Hui-Min Shen, Jing-Ping Yun, Li-Li Liu","doi":"10.1038/s41418-025-01500-z","DOIUrl":"https://doi.org/10.1038/s41418-025-01500-z","url":null,"abstract":"<p>Ovarian cancer (OC) is a highly fatal and refractory malignancy affecting women, and platinum resistance remains a major clinical dilemma. Compared with other OC subtypes, ovarian clear cell carcinoma (OCCC) frequently exhibits increased platinum refractoriness, accompanied by increased glycogen levels, which promotes clear-cell morphology, and wild-type p53. However, the roles of these factors in platinum resistance of OCCC are unclear. Here, we investigated whether glycogen promotes OCCC resistance to platinum agents and reported that GYS1, a rate-limiting enzyme in glycogen synthesis, is clinically associated with poor prognosis and chemoresistance in OCCC. Mechanistically, p53 promotes GYS1 breakdown via the upregulation of RNF144a, whereas GYS1 induces the reversal of p53 ubiquitination and degradation by competitively binding to USP14, forming a positive feedback circuit. Under platinum stress, the accumulated glycogen is mobilized by the p53/GYS1 feedback circuit, which fuels energetic NADPH production, resulting in resistance to disulfidptosis and increased platinum resistance in OCCC. Collectively, our findings identify glycogen as a contributor to OCCC platinum resistance and elucidate the underlying mechanisms, highlighting a crucial p53/GYS1 positive feedback loop.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"183 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}