Pub Date : 2025-10-07DOI: 10.1038/s41556-025-01783-x
Ageing and cancer are often seen as divergent tissue fates. In our study, we identify a protective programme, called senescence-coupled differentiation (or seno-differentiation), that eliminates cancer-prone stem cells by pushing them to differentiate. Whether melanocyte stem cells follow this path or bypass it under carcinogenic stress determines tissue outcomes: hair greying or melanoma development.
{"title":"Senescence-coupled differentiation selectively eliminates cancer-prone stem cells","authors":"","doi":"10.1038/s41556-025-01783-x","DOIUrl":"10.1038/s41556-025-01783-x","url":null,"abstract":"Ageing and cancer are often seen as divergent tissue fates. In our study, we identify a protective programme, called senescence-coupled differentiation (or seno-differentiation), that eliminates cancer-prone stem cells by pushing them to differentiate. Whether melanocyte stem cells follow this path or bypass it under carcinogenic stress determines tissue outcomes: hair greying or melanoma development.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1605-1606"},"PeriodicalIF":19.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241097","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}
Pub Date : 2025-10-07DOI: 10.1038/s41556-025-01765-z
Naomi R. Genuth, Andrew Dillin
Organisms must constantly respond to stress to maintain homeostasis, and the successful implementation of cellular stress responses is directly linked to lifespan regulation. In this Review we examine how three age-associated stressors—loss of proteostasis, oxidative damage and dysregulated nutrient sensing—alter protein synthesis. We describe how these stressors inflict cellular damage via their effects on translation and how translational changes can serve as both sensors and responses to the stressor. Finally, we compare stress-induced translational programmes to protein synthesis alterations that occur with age and discuss whether these changes are adaptive or deleterious to longevity and healthy ageing. This Review discusses the effects of three age-associated stressors—loss of proteostasis, oxidative damage and dysregulated nutrient sensing—on global protein synthesis and highlights how altered translation is used by the cell as a stress sensor.
{"title":"Translational regulation in stress biology","authors":"Naomi R. Genuth, Andrew Dillin","doi":"10.1038/s41556-025-01765-z","DOIUrl":"10.1038/s41556-025-01765-z","url":null,"abstract":"Organisms must constantly respond to stress to maintain homeostasis, and the successful implementation of cellular stress responses is directly linked to lifespan regulation. In this Review we examine how three age-associated stressors—loss of proteostasis, oxidative damage and dysregulated nutrient sensing—alter protein synthesis. We describe how these stressors inflict cellular damage via their effects on translation and how translational changes can serve as both sensors and responses to the stressor. Finally, we compare stress-induced translational programmes to protein synthesis alterations that occur with age and discuss whether these changes are adaptive or deleterious to longevity and healthy ageing. This Review discusses the effects of three age-associated stressors—loss of proteostasis, oxidative damage and dysregulated nutrient sensing—on global protein synthesis and highlights how altered translation is used by the cell as a stress sensor.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1609-1621"},"PeriodicalIF":19.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244798","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}
Pub Date : 2025-10-06DOI: 10.1038/s41556-025-01769-9
Yasuaki Mohri, Jialiang Nie, Hironobu Morinaga, Tomoki Kato, Takahiro Aoto, Takashi Yamanashi, Daisuke Nanba, Hiroyuki Matsumura, Sakura Kirino, Kouji Kobiyama, Ken J. Ishii, Masahiro Hayashi, Tamio Suzuki, Takeshi Namiki, Jun Seita, Emi K. Nishimura
The exposome, an individual’s lifelong environmental exposure, profoundly impacts health. Somatic tissues undergo functional decline with age, exhibiting characteristic ageing phenotypes, including hair greying and cancer. However, the specific genotoxins, signals and cellular mechanisms underlying each phenotype remain largely unknown. Here we report that melanocyte stem cells (McSCs) and their niche coordinately determine individual stem cell fate through antagonistic, stress-responsive pathways, depending on the type of genotoxic damage incurred. McSC fate tracking in mice revealed that McSCs undergo cellular senescence-coupled differentiation (seno-differentiation) in response to DNA double-strand breaks, resulting in their selective depletion and hair greying, and effectively protecting against melanoma. Conversely, carcinogens can suppress McSC seno-differentiation, even in cells harbouring double-strand breaks, by activating arachidonic acid metabolism and the niche-derived KIT ligand, thereby promoting McSC self-renewal. Collectively, the fate of individual stem cell clones—expansion versus exhaustion—cumulatively and antagonistically governs ageing phenotypes through interaction with the niche. Mohri et al. show that, in response to genotoxic stress, melanocyte stem cells undergo senescence-associated differentiation, causing their depletion and protecting them against melanomagenesis. This process is suppressed by carcinogens.
{"title":"Antagonistic stem cell fates under stress govern decisions between hair greying and melanoma","authors":"Yasuaki Mohri, Jialiang Nie, Hironobu Morinaga, Tomoki Kato, Takahiro Aoto, Takashi Yamanashi, Daisuke Nanba, Hiroyuki Matsumura, Sakura Kirino, Kouji Kobiyama, Ken J. Ishii, Masahiro Hayashi, Tamio Suzuki, Takeshi Namiki, Jun Seita, Emi K. Nishimura","doi":"10.1038/s41556-025-01769-9","DOIUrl":"10.1038/s41556-025-01769-9","url":null,"abstract":"The exposome, an individual’s lifelong environmental exposure, profoundly impacts health. Somatic tissues undergo functional decline with age, exhibiting characteristic ageing phenotypes, including hair greying and cancer. However, the specific genotoxins, signals and cellular mechanisms underlying each phenotype remain largely unknown. Here we report that melanocyte stem cells (McSCs) and their niche coordinately determine individual stem cell fate through antagonistic, stress-responsive pathways, depending on the type of genotoxic damage incurred. McSC fate tracking in mice revealed that McSCs undergo cellular senescence-coupled differentiation (seno-differentiation) in response to DNA double-strand breaks, resulting in their selective depletion and hair greying, and effectively protecting against melanoma. Conversely, carcinogens can suppress McSC seno-differentiation, even in cells harbouring double-strand breaks, by activating arachidonic acid metabolism and the niche-derived KIT ligand, thereby promoting McSC self-renewal. Collectively, the fate of individual stem cell clones—expansion versus exhaustion—cumulatively and antagonistically governs ageing phenotypes through interaction with the niche. Mohri et al. show that, in response to genotoxic stress, melanocyte stem cells undergo senescence-associated differentiation, causing their depletion and protecting them against melanomagenesis. This process is suppressed by carcinogens.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1647-1659"},"PeriodicalIF":19.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145235667","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}
Pub Date : 2025-10-03DOI: 10.1038/s41556-025-01782-y
Andrea Fratton, Boyan Bonev
The regulatory mechanisms that drive oncogene expression in gliomas remain poorly understood. A study now identifies a role for widespread rearrangements of the enhancer connectome. Such rearrangements are linked to known genetic risk variants, revealing how genetic predisposition contributes to malignancy.
{"title":"Deciphering glioma susceptibility","authors":"Andrea Fratton, Boyan Bonev","doi":"10.1038/s41556-025-01782-y","DOIUrl":"10.1038/s41556-025-01782-y","url":null,"abstract":"The regulatory mechanisms that drive oncogene expression in gliomas remain poorly understood. A study now identifies a role for widespread rearrangements of the enhancer connectome. Such rearrangements are linked to known genetic risk variants, revealing how genetic predisposition contributes to malignancy.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1603-1604"},"PeriodicalIF":19.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225592","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}
Pub Date : 2025-10-03DOI: 10.1038/s41556-025-01755-1
Tianze Wang, Yan Pan, Fusong Ju, Shuxin Zheng, Chang Liu, Yaosen Min, Qun Jiang, Xinwei Liu, Huanhuan Xia, Guoqing Liu, Haiguang Liu, Pan Deng
A select few genes act as pivotal drivers in the process of cell state transitions. However, finding key genes involved in different transitions is challenging. Here, to address this problem, we present CellNavi, a deep learning-based framework designed to predict genes that drive cell state transitions. CellNavi builds a driver gene predictor upon a cell state manifold, which captures the intrinsic features of cells by learning from large-scale, high-dimensional transcriptomics data and integrating gene graphs with directional connections. Our analysis shows that CellNavi can accurately predict driver genes for transitions induced by genetic, chemical and cytokine perturbations across diverse cell types, conditions and studies. By leveraging a biologically meaningful cell state manifold, it is proficient in tasks involving critical transitions such as cellular differentiation, disease progression and drug response. CellNavi represents a substantial advancement in driver gene prediction and cell state manipulation, opening new avenues in disease biology and therapeutic discovery. The authors integrate single-cell transcriptomic data with prior gene graphs to produce a biologically meaningful cell state manifold that can predict driver genes for genetic perturbations and differentiation events across diverse cell types.
{"title":"CellNavi predicts genes directing cellular transitions by learning a gene graph-enhanced cell state manifold","authors":"Tianze Wang, Yan Pan, Fusong Ju, Shuxin Zheng, Chang Liu, Yaosen Min, Qun Jiang, Xinwei Liu, Huanhuan Xia, Guoqing Liu, Haiguang Liu, Pan Deng","doi":"10.1038/s41556-025-01755-1","DOIUrl":"10.1038/s41556-025-01755-1","url":null,"abstract":"A select few genes act as pivotal drivers in the process of cell state transitions. However, finding key genes involved in different transitions is challenging. Here, to address this problem, we present CellNavi, a deep learning-based framework designed to predict genes that drive cell state transitions. CellNavi builds a driver gene predictor upon a cell state manifold, which captures the intrinsic features of cells by learning from large-scale, high-dimensional transcriptomics data and integrating gene graphs with directional connections. Our analysis shows that CellNavi can accurately predict driver genes for transitions induced by genetic, chemical and cytokine perturbations across diverse cell types, conditions and studies. By leveraging a biologically meaningful cell state manifold, it is proficient in tasks involving critical transitions such as cellular differentiation, disease progression and drug response. CellNavi represents a substantial advancement in driver gene prediction and cell state manipulation, opening new avenues in disease biology and therapeutic discovery. The authors integrate single-cell transcriptomic data with prior gene graphs to produce a biologically meaningful cell state manifold that can predict driver genes for genetic perturbations and differentiation events across diverse cell types.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1863-1874"},"PeriodicalIF":19.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41556-025-01755-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145215950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-01DOI: 10.1038/s41556-025-01773-z
Giada Vanni, Anna Citron, Ambela Suli, Paolo Contessotto, Robin Caire, Alessandro Gandin, Giovanna Mantovan, Francesca Zanconato, Giovanna Brusatin, Michele Di Palma, Elisa Peirano, Lisa Sofia Pozzer, Carlo Albanese Jr, Roberto A. Steiner, Michelangelo Cordenonsi, Tito Panciera, Stefano Piccolo
Cellular mechanotransduction is a key informational system, yet its mechanisms remain elusive. Here we unveil the role of microtubules in mechanosignalling, operating downstream of subnuclear F-actin and nuclear envelope mechanics. Upon mechanical activation, microtubules reorganize from a perinuclear cage into a radial array nucleated by centrosomes. This structural rearrangement triggers degradation of AMOT proteins, which we identify as key mechanical rheostats that sequester YAP/TAZ in the cytoplasm. AMOT is stable in mechano-OFF but degraded in mechano-ON cell states, where microtubules allow AMOT rapid transport to the pericentrosomal proteasome in complex with dynein/dynactin. This process ensures swift control of YAP/TAZ function in response to changes in cell mechanics, with experimental loss of AMOT proteins rendering cells insensitive to mechanical modulations. Ras/RTK oncogenes promote YAP/TAZ-dependent tumorigenesis by corrupting this AMOT-centred mechanical checkpoint. Notably, the Hippo pathway fine-tunes mechanotransduction: LATS kinases phosphorylate AMOT, shielding it from degradation, thereby indirectly restraining YAP/TAZ. Thus, AMOT protein stability serves as a hub linking cytoskeletal reorganization and Hippo signalling to YAP/TAZ mechanosignalling. Vanni et al. show a role for microtubules in YAP/TAZ mechanosignalling. Mechanoresponsive microtubule reorganization into centrosomal arrays allows for AMOT delivery to pericentrosomal proteasomes and degradation, leading to YAP/TAZ activation.
{"title":"Microtubule architecture connects AMOT stability to YAP/TAZ mechanotransduction and Hippo signalling","authors":"Giada Vanni, Anna Citron, Ambela Suli, Paolo Contessotto, Robin Caire, Alessandro Gandin, Giovanna Mantovan, Francesca Zanconato, Giovanna Brusatin, Michele Di Palma, Elisa Peirano, Lisa Sofia Pozzer, Carlo Albanese Jr, Roberto A. Steiner, Michelangelo Cordenonsi, Tito Panciera, Stefano Piccolo","doi":"10.1038/s41556-025-01773-z","DOIUrl":"10.1038/s41556-025-01773-z","url":null,"abstract":"Cellular mechanotransduction is a key informational system, yet its mechanisms remain elusive. Here we unveil the role of microtubules in mechanosignalling, operating downstream of subnuclear F-actin and nuclear envelope mechanics. Upon mechanical activation, microtubules reorganize from a perinuclear cage into a radial array nucleated by centrosomes. This structural rearrangement triggers degradation of AMOT proteins, which we identify as key mechanical rheostats that sequester YAP/TAZ in the cytoplasm. AMOT is stable in mechano-OFF but degraded in mechano-ON cell states, where microtubules allow AMOT rapid transport to the pericentrosomal proteasome in complex with dynein/dynactin. This process ensures swift control of YAP/TAZ function in response to changes in cell mechanics, with experimental loss of AMOT proteins rendering cells insensitive to mechanical modulations. Ras/RTK oncogenes promote YAP/TAZ-dependent tumorigenesis by corrupting this AMOT-centred mechanical checkpoint. Notably, the Hippo pathway fine-tunes mechanotransduction: LATS kinases phosphorylate AMOT, shielding it from degradation, thereby indirectly restraining YAP/TAZ. Thus, AMOT protein stability serves as a hub linking cytoskeletal reorganization and Hippo signalling to YAP/TAZ mechanosignalling. Vanni et al. show a role for microtubules in YAP/TAZ mechanosignalling. Mechanoresponsive microtubule reorganization into centrosomal arrays allows for AMOT delivery to pericentrosomal proteasomes and degradation, leading to YAP/TAZ activation.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1725-1738"},"PeriodicalIF":19.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41556-025-01773-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-01DOI: 10.1038/s41556-025-01776-w
Yanhe Li, Jincan He, Yingdong Liu, Yi Hui, Shanyao Liu, Yalin Zhang, Yan Xiong, Tingting Xu, Ziwen Xu, Zhuoao Zhang, Yan Zhang, Guang Yang, Jia Zhao, Dandan Bai, Xinyi Lei, Xiaochen Kou, Yanhong Zhao, Jing Du, Zheng Guo, Jiqing Yin, Xiaoqing Zhang, Congling Xu, Yawei Gao, Miaoxin Chen, Hong Wang, Cizhong Jiang, Shaorong Gao, Wenqiang Liu
Bivalency regulates developmental genes during lineage commitment. However, mechanisms governing bivalent domain establishment, maintenance and resolution in early embryogenesis remain unclear. Here we comprehensively trace bivalent chromatin remodelling throughout mouse peri-implantation development, revealing bifurcated establishment modes that partition epiblast and primitive endoderm regulatory programmes. We identify transiently maintained bivalent domains (TB domains) enriched in the epiblast, where gradual resolution fine-tunes pluripotency progression. Through targeted screening in embryos, we uncover 22 TB domain regulators, including the essential factor ZBTB17. Genetic ablation or degradation of ZBTB17 causes peri-implantation arrest. Mechanistically, ZBTB17 collaborates with KDM6A/B to resolve bivalency by removing H3K27me3 and priming the activation of key pluripotency genes. Remarkably, TB domain dynamics are evolutionarily shared in human pluripotent transitions, with ZBTB17 involvement despite species differences. Our work establishes a framework for bivalent chromatin regulation in early mammalian development and elucidates how its resolution precisely controls lineage commitment. Li, He, Liu and colleagues characterize the dynamic bivalent chromatin landscape during mouse peri-implantation development. They find that factor ZBTB17 works with KDM6A/B to resolve transiently maintained bivalent domains and prime gene activation.
{"title":"Remodelling bivalent chromatin is essential for mouse peri-implantation embryogenesis","authors":"Yanhe Li, Jincan He, Yingdong Liu, Yi Hui, Shanyao Liu, Yalin Zhang, Yan Xiong, Tingting Xu, Ziwen Xu, Zhuoao Zhang, Yan Zhang, Guang Yang, Jia Zhao, Dandan Bai, Xinyi Lei, Xiaochen Kou, Yanhong Zhao, Jing Du, Zheng Guo, Jiqing Yin, Xiaoqing Zhang, Congling Xu, Yawei Gao, Miaoxin Chen, Hong Wang, Cizhong Jiang, Shaorong Gao, Wenqiang Liu","doi":"10.1038/s41556-025-01776-w","DOIUrl":"10.1038/s41556-025-01776-w","url":null,"abstract":"Bivalency regulates developmental genes during lineage commitment. However, mechanisms governing bivalent domain establishment, maintenance and resolution in early embryogenesis remain unclear. Here we comprehensively trace bivalent chromatin remodelling throughout mouse peri-implantation development, revealing bifurcated establishment modes that partition epiblast and primitive endoderm regulatory programmes. We identify transiently maintained bivalent domains (TB domains) enriched in the epiblast, where gradual resolution fine-tunes pluripotency progression. Through targeted screening in embryos, we uncover 22 TB domain regulators, including the essential factor ZBTB17. Genetic ablation or degradation of ZBTB17 causes peri-implantation arrest. Mechanistically, ZBTB17 collaborates with KDM6A/B to resolve bivalency by removing H3K27me3 and priming the activation of key pluripotency genes. Remarkably, TB domain dynamics are evolutionarily shared in human pluripotent transitions, with ZBTB17 involvement despite species differences. Our work establishes a framework for bivalent chromatin regulation in early mammalian development and elucidates how its resolution precisely controls lineage commitment. Li, He, Liu and colleagues characterize the dynamic bivalent chromatin landscape during mouse peri-implantation development. They find that factor ZBTB17 works with KDM6A/B to resolve transiently maintained bivalent domains and prime gene activation.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1797-1811"},"PeriodicalIF":19.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203555","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}
Pub Date : 2025-09-30DOI: 10.1038/s41556-025-01780-0
Yonglong Dang, Yuk Kit Lor, Gonçalo Castelo-Branco
Glioblastoma (GBM) heterogeneity might arise because of the activation of various gene core regulatory circuitries (CRCs). A new study highlights the central role of HOXB3 in GBM CRCs and how peptide-mediated perturbation of HOXB3-related CRCs in GBM holds potential as treatment for a subset of patients.
{"title":"Cracking glioblastoma core regulatory codes","authors":"Yonglong Dang, Yuk Kit Lor, Gonçalo Castelo-Branco","doi":"10.1038/s41556-025-01780-0","DOIUrl":"10.1038/s41556-025-01780-0","url":null,"abstract":"Glioblastoma (GBM) heterogeneity might arise because of the activation of various gene core regulatory circuitries (CRCs). A new study highlights the central role of HOXB3 in GBM CRCs and how peptide-mediated perturbation of HOXB3-related CRCs in GBM holds potential as treatment for a subset of patients.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 10","pages":"1600-1602"},"PeriodicalIF":19.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200369","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}
Pub Date : 2025-09-30DOI: 10.1038/s41556-025-01791-x
Georgia Chatzinikolaou, Zivkos Apostolou, Tamara Aid-Pavlidis, Anna Ioannidou, Ismene Karakasilioti, Giorgio L. Papadopoulos, Michalis Aivaliotis, Maria Tsekrekou, John Strouboulis, Theodore Kosteas, George A. Garinis
{"title":"Author Correction: ERCC1–XPF cooperates with CTCF and cohesin to facilitate the developmental silencing of imprinted genes","authors":"Georgia Chatzinikolaou, Zivkos Apostolou, Tamara Aid-Pavlidis, Anna Ioannidou, Ismene Karakasilioti, Giorgio L. Papadopoulos, Michalis Aivaliotis, Maria Tsekrekou, John Strouboulis, Theodore Kosteas, George A. Garinis","doi":"10.1038/s41556-025-01791-x","DOIUrl":"10.1038/s41556-025-01791-x","url":null,"abstract":"","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 12","pages":"2240-2240"},"PeriodicalIF":19.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41556-025-01791-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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