Pub Date : 2026-01-28DOI: 10.1038/s41422-026-01222-y
Qing Ma, Wenjun Xu, Xuan Wang, Haoyu Nie, Yukun Gao, Rui Hu, Zhihao Yang, Xushu Wang, Ta Na, Xiangyi Chen, Zhaoyue Wang, Minglu Xu, Li Shao, Meng Guo, Yanfang Liu, Rongrong Le, Shaorong Gao, Weida Li
Pancreatic β-cell identity loss is increasingly recognized as a critical pathogenic contributor to β-cell failure in type 2 diabetes (T2D), but the specific mechanism remains to be characterized. In this study, we demonstrate that zinc accumulation contributes to β-cell identity loss during diabetes progression in both human and mouse islets. Using a model of human embryonic stem cell-derived islets (SC-islets), we reveal that accumulated zinc triggers the integrated stress response (ISR), with elevated ATF4 expression in SC-β cells. This, in turn, initiates expression of the α cell-specific transcription factor ARX, resulting in the conversion of β cells to α cells, thus forming a zinc-ATF4-ARX regulatory axis. Like primary β cells, SC-β cells also undergo identity loss after transplantation into diabetic animals, which can be prevented by an ISR inhibitor, resulting in improved glycemic control. Furthermore, both genetic depletion and chemical inhibition of zinc accumulation effectively safeguard SC-β cells from identity loss and enhance their efficacy in diabetic animals. Our study thus reveals a pathogenic mechanism in which zinc accumulation induces β-cell identity loss through lineage-tracing approaches and proposes a protective strategy to counteract this process.
{"title":"Zinc accumulation-induced integrated stress response triggers β-cell identity loss","authors":"Qing Ma, Wenjun Xu, Xuan Wang, Haoyu Nie, Yukun Gao, Rui Hu, Zhihao Yang, Xushu Wang, Ta Na, Xiangyi Chen, Zhaoyue Wang, Minglu Xu, Li Shao, Meng Guo, Yanfang Liu, Rongrong Le, Shaorong Gao, Weida Li","doi":"10.1038/s41422-026-01222-y","DOIUrl":"https://doi.org/10.1038/s41422-026-01222-y","url":null,"abstract":"Pancreatic β-cell identity loss is increasingly recognized as a critical pathogenic contributor to β-cell failure in type 2 diabetes (T2D), but the specific mechanism remains to be characterized. In this study, we demonstrate that zinc accumulation contributes to β-cell identity loss during diabetes progression in both human and mouse islets. Using a model of human embryonic stem cell-derived islets (SC-islets), we reveal that accumulated zinc triggers the integrated stress response (ISR), with elevated ATF4 expression in SC-β cells. This, in turn, initiates expression of the α cell-specific transcription factor ARX, resulting in the conversion of β cells to α cells, thus forming a zinc-ATF4-ARX regulatory axis. Like primary β cells, SC-β cells also undergo identity loss after transplantation into diabetic animals, which can be prevented by an ISR inhibitor, resulting in improved glycemic control. Furthermore, both genetic depletion and chemical inhibition of zinc accumulation effectively safeguard SC-β cells from identity loss and enhance their efficacy in diabetic animals. Our study thus reveals a pathogenic mechanism in which zinc accumulation induces β-cell identity loss through lineage-tracing approaches and proposes a protective strategy to counteract this process.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"296 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146057207","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}
Methionine metabolism generates the substrate S-adenosylmethionine (SAM), which regulates epigenetic modifications crucial for various cellular processes, particularly tumorigenesis. However, whether methionine metabolism involves epigenetic mechanisms independent of SAM and what roles such mechanisms play in tumorigenesis remain unclear. We show here that the adenosylhomocysteinase (AHCY)–adenosine complex increases mRNA m6A levels in a non-global manner, promoting fatty acid synthesis and tumorigenesis. Adenosine increases mRNA m6A levels by binding to the methionine metabolism enzyme AHCY to form a complex, rather than depending on adenosine receptors. The AHCY–adenosine complex facilitates AHCY dimerization, with adenosine being crucial for dimer stability. AHCY dimers hinder the binding of fat mass and obesity-associated protein (FTO) at the Q86 site to RNA containing the VWDRACH motif, increasing m6A levels and upregulating lipogenesis genes, especially ACACA and SCD1, thus leading to reprogramming of lipid metabolism. Conversely, AHCY mutants that have lost dimerization or FTO-binding ability but retain hydrolase activity suppress lipogenesis and tumor growth without significantly affecting methionine catabolism mediated by AHCY. Loss of AHCY in mice and disruption of AHCY dimerization in tumor cells and patient-derived xenograft models restricted tumor growth. Our findings demonstrate a key SAM-independent link between methionine metabolism and mRNA m6A modification that affects demethylase substrate specificity. This novel link between the methionine cycle and lipid metabolism suggests new strategies for anticancer therapy.
{"title":"The AHCY–adenosine complex rewires mRNA methylation to enhance fatty acid biosynthesis and tumorigenesis","authors":"Kun Liao, Fen Cao, Chen Wei, Zheng-Yu Qian, Hong-Rong Hu, Wen-Feng Pan, Zi-Qing Feng, Sen-mao Lian, Zi-Xuan Xiao, Hui Sheng, Hai-Yu Mo, Yi-Xuan Zhao, Qi-Nian Wu, Zhao-Lei Zeng, Bo Li, Rui-Hua Xu, Huai-Qiang Ju","doi":"10.1038/s41422-025-01213-5","DOIUrl":"10.1038/s41422-025-01213-5","url":null,"abstract":"Methionine metabolism generates the substrate S-adenosylmethionine (SAM), which regulates epigenetic modifications crucial for various cellular processes, particularly tumorigenesis. However, whether methionine metabolism involves epigenetic mechanisms independent of SAM and what roles such mechanisms play in tumorigenesis remain unclear. We show here that the adenosylhomocysteinase (AHCY)–adenosine complex increases mRNA m6A levels in a non-global manner, promoting fatty acid synthesis and tumorigenesis. Adenosine increases mRNA m6A levels by binding to the methionine metabolism enzyme AHCY to form a complex, rather than depending on adenosine receptors. The AHCY–adenosine complex facilitates AHCY dimerization, with adenosine being crucial for dimer stability. AHCY dimers hinder the binding of fat mass and obesity-associated protein (FTO) at the Q86 site to RNA containing the VWDRACH motif, increasing m6A levels and upregulating lipogenesis genes, especially ACACA and SCD1, thus leading to reprogramming of lipid metabolism. Conversely, AHCY mutants that have lost dimerization or FTO-binding ability but retain hydrolase activity suppress lipogenesis and tumor growth without significantly affecting methionine catabolism mediated by AHCY. Loss of AHCY in mice and disruption of AHCY dimerization in tumor cells and patient-derived xenograft models restricted tumor growth. Our findings demonstrate a key SAM-independent link between methionine metabolism and mRNA m6A modification that affects demethylase substrate specificity. This novel link between the methionine cycle and lipid metabolism suggests new strategies for anticancer therapy.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"36 2","pages":"152-172"},"PeriodicalIF":25.9,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41422-025-01213-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993482","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 : 2026-01-14DOI: 10.1038/s41422-025-01212-6
Andrew Allan Almonte, Simon Thomas, Valerio Iebba, Guido Kroemer, Lisa Derosa, Laurence Zitvogel
The gut microbiome is recognized as a determinant of response to immune checkpoint inhibitor (ICI) therapies in cancer. However, the clinical translation of microbiome science has been hampered by inconsistent definitions of dysbiosis, inadequate biomarker frameworks, and limited mechanistic understanding. In this review, we synthesize the current state of knowledge on how gut microbial composition and function influence ICI efficacy, highlighting both correlative and causal evidence. We discuss computational approaches based on α-diversity or taxonomic abundance and argue for more functionally and clinically informative models, such as the topological score (TOPOSCORE) and other dysbiosis indices derived from machine learning. Using retrospective analyses of metagenomic datasets from thousands of patients and healthy controls, we examine microbial patterns that distinguish responders from non-responders. We also explore how dysbiosis perturbs immunoregulatory pathways, including bile acid metabolism, gut permeability, and mucosal immunomodulation. Finally, we assess emerging therapeutic strategies aimed at correcting microbiome dysfunction — including dietary modification, bacterial consortia, and fecal microbiota transplantation — and describe how they are being deployed in multiple clinical trials. We conclude with a brief discussion of the ONCOBIOME initiative, which works with international partners to incorporate microbiome science into oncology workflows. By refining our understanding of gut–immune interactions and translating it into action, microbiome-informed oncology may unlock new therapeutic potential for patients previously resistant to immunotherapy.
{"title":"Gut dysbiosis in oncology: a risk factor for immunoresistance","authors":"Andrew Allan Almonte, Simon Thomas, Valerio Iebba, Guido Kroemer, Lisa Derosa, Laurence Zitvogel","doi":"10.1038/s41422-025-01212-6","DOIUrl":"10.1038/s41422-025-01212-6","url":null,"abstract":"The gut microbiome is recognized as a determinant of response to immune checkpoint inhibitor (ICI) therapies in cancer. However, the clinical translation of microbiome science has been hampered by inconsistent definitions of dysbiosis, inadequate biomarker frameworks, and limited mechanistic understanding. In this review, we synthesize the current state of knowledge on how gut microbial composition and function influence ICI efficacy, highlighting both correlative and causal evidence. We discuss computational approaches based on α-diversity or taxonomic abundance and argue for more functionally and clinically informative models, such as the topological score (TOPOSCORE) and other dysbiosis indices derived from machine learning. Using retrospective analyses of metagenomic datasets from thousands of patients and healthy controls, we examine microbial patterns that distinguish responders from non-responders. We also explore how dysbiosis perturbs immunoregulatory pathways, including bile acid metabolism, gut permeability, and mucosal immunomodulation. Finally, we assess emerging therapeutic strategies aimed at correcting microbiome dysfunction — including dietary modification, bacterial consortia, and fecal microbiota transplantation — and describe how they are being deployed in multiple clinical trials. We conclude with a brief discussion of the ONCOBIOME initiative, which works with international partners to incorporate microbiome science into oncology workflows. By refining our understanding of gut–immune interactions and translating it into action, microbiome-informed oncology may unlock new therapeutic potential for patients previously resistant to immunotherapy.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"36 2","pages":"103-120"},"PeriodicalIF":25.9,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41422-025-01212-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968492","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 : 2026-01-13DOI: 10.1038/s41422-025-01207-3
Yaxin Niu, Shengmin Hu, Yanfeng Zhang, Jinbao Yang, Jiarui Zhang, Ruiping He, Li Chen, Lin Xu, Hongfang Zhao, Bing Gan, Ruobing Ren, Ruth J. F. Loos, Haobin Ye, Xingrong Du, Tongjin Zhao, Peng Li, Antonio Vidal-Puig, Linzhang Huang
Insulin-stimulated glucose uptake is central to global carbohydrate metabolism, yet metabolites that enhance glucose uptake independently of insulin remain undefined. Here, we identify L-lactate as an insulin-independent regulator of glucose uptake that mitigates hyperglycemia. Loss of LDHA in muscle reduces lactate production, impairing glucose homeostasis in mice. By contrast, lactate administration or genetic upregulation of lactate production improves glucose control. Knockout of the lactate receptor GPR81 in skeletal muscle worsens glucose tolerance, whereas its ectopic expression or pharmacological activation enhances carbohydrate metabolism. Mechanistically, GPR81 recruits FARP1 to activate RAC1, promoting GLUT4 translocation independently of insulin signaling. Notably, the expression of LDHA, GPR81, and FARP1 is upregulated after exercise, and GPR81 variants are highly correlated with fasting insulin levels in humans, underscoring the synergy of the GPR81-FARP1-GLUT4 axis with insulin in glucose regulation. Our findings suggest that targeting GPR81 represents a potential insulin-independent strategy for the treatment of hyperglycemia.
{"title":"Lactate-activated GPR81/FARP1 signaling drives insulin-independent glucose uptake and metabolic control","authors":"Yaxin Niu, Shengmin Hu, Yanfeng Zhang, Jinbao Yang, Jiarui Zhang, Ruiping He, Li Chen, Lin Xu, Hongfang Zhao, Bing Gan, Ruobing Ren, Ruth J. F. Loos, Haobin Ye, Xingrong Du, Tongjin Zhao, Peng Li, Antonio Vidal-Puig, Linzhang Huang","doi":"10.1038/s41422-025-01207-3","DOIUrl":"10.1038/s41422-025-01207-3","url":null,"abstract":"Insulin-stimulated glucose uptake is central to global carbohydrate metabolism, yet metabolites that enhance glucose uptake independently of insulin remain undefined. Here, we identify L-lactate as an insulin-independent regulator of glucose uptake that mitigates hyperglycemia. Loss of LDHA in muscle reduces lactate production, impairing glucose homeostasis in mice. By contrast, lactate administration or genetic upregulation of lactate production improves glucose control. Knockout of the lactate receptor GPR81 in skeletal muscle worsens glucose tolerance, whereas its ectopic expression or pharmacological activation enhances carbohydrate metabolism. Mechanistically, GPR81 recruits FARP1 to activate RAC1, promoting GLUT4 translocation independently of insulin signaling. Notably, the expression of LDHA, GPR81, and FARP1 is upregulated after exercise, and GPR81 variants are highly correlated with fasting insulin levels in humans, underscoring the synergy of the GPR81-FARP1-GLUT4 axis with insulin in glucose regulation. Our findings suggest that targeting GPR81 represents a potential insulin-independent strategy for the treatment of hyperglycemia.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"36 2","pages":"137-151"},"PeriodicalIF":25.9,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956283","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 : 2026-01-13DOI: 10.1038/s41422-025-01215-3
Jaiya Randhawa,Luke A J O'Neill
{"title":"Mitochondria target the plasma membrane to cause mitoxyperiosis.","authors":"Jaiya Randhawa,Luke A J O'Neill","doi":"10.1038/s41422-025-01215-3","DOIUrl":"https://doi.org/10.1038/s41422-025-01215-3","url":null,"abstract":"","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"26 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961333","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 : 2026-01-09DOI: 10.1038/s41422-025-01214-4
Zhi Cheng, Bryan L. Roth
{"title":"Gz and β-arrestin 1 signaling in the μ-opioid receptor","authors":"Zhi Cheng, Bryan L. Roth","doi":"10.1038/s41422-025-01214-4","DOIUrl":"10.1038/s41422-025-01214-4","url":null,"abstract":"","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"36 2","pages":"97-98"},"PeriodicalIF":25.9,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41422-025-01214-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932511","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}
Achieving long-term ex vivo expansion of functional hematopoietic stem cells (HSCs) is essential for advancing HSC-based clinical therapies. Although mechanosensitive ion channels are known to play key roles in the hematopoietic system, their involvement in HSC expansion remains unclear. Here, we show that Piezo1 is highly expressed in HSCs. Both genetic deletion and prolonged chemical activation of Piezo1 impair cultured HSC function, indicating that transient mechanical activation of Piezo1 is required for maintenance of HSCs in culture. To achieve this, we screened various microspheres and found that PS500 (500-nm polystyrene microspheres) significantly enhanced ex vivo expansion of mouse bone marrow HSCs with long-term repopulating capacity. PS500 also expanded human umbilical cord blood HSCs capable of engraftment in immunodeficient mice. Mechanistically, PS500 activates Piezo1, triggering Ca2+-dependent expression of proliferative cytokines and subsequent STAT3 activation, which support HSC self-renewal and proliferation. Together, these findings show that PS500 enables transient Piezo1 activation and efficient, non-toxic expansion of functional HSCs, offering a promising approach for the generation of transplantable HSCs for clinical use.
{"title":"Transient mechanical activation of the Piezo1 channel facilitates ex vivo expansion of hematopoietic stem cells","authors":"Qiwei Wang, Xin Zeng, Haoxiang Yang, Huan Lu, Lingli Jiang, Lizhen Xu, Jinxin Li, Jingyi Li, Yingli Han, Xiaoyan Wu, Yuanhong Zhou, Xiaolan Chen, Yanmin Zhao, Jimin Shi, Yi Luo, Fang Ni, Jie Sun, Qian Zhao, Fan Yang, Peng Xia, Hongyuan Jiang, He Huang, Pengxu Qian","doi":"10.1038/s41422-025-01209-1","DOIUrl":"https://doi.org/10.1038/s41422-025-01209-1","url":null,"abstract":"Achieving long-term ex vivo expansion of functional hematopoietic stem cells (HSCs) is essential for advancing HSC-based clinical therapies. Although mechanosensitive ion channels are known to play key roles in the hematopoietic system, their involvement in HSC expansion remains unclear. Here, we show that Piezo1 is highly expressed in HSCs. Both genetic deletion and prolonged chemical activation of Piezo1 impair cultured HSC function, indicating that transient mechanical activation of Piezo1 is required for maintenance of HSCs in culture. To achieve this, we screened various microspheres and found that PS500 (500-nm polystyrene microspheres) significantly enhanced ex vivo expansion of mouse bone marrow HSCs with long-term repopulating capacity. PS500 also expanded human umbilical cord blood HSCs capable of engraftment in immunodeficient mice. Mechanistically, PS500 activates Piezo1, triggering Ca2+-dependent expression of proliferative cytokines and subsequent STAT3 activation, which support HSC self-renewal and proliferation. Together, these findings show that PS500 enables transient Piezo1 activation and efficient, non-toxic expansion of functional HSCs, offering a promising approach for the generation of transplantable HSCs for clinical use.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"22 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145919921","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}
R-loops are pervasive genomic structures that link epigenetic modification and transcriptional regulation. However, the functional roles and regulatory mechanisms of R-loops during preimplantation development in mammals remain unexplored. Here, we reveal that the reprogramming of R-loops across developmental stages depends on CG density, with CG-poor R-loops more stage specific and strongly associated with early embryonic development. Loss of CG-poor R-loops causes severe defects in the maternal-to-zygotic transition (MZT) and preimplantation embryo development. This abnormal maintenance of CG-poor R-loops promotes premature activation of major zygotic genome activation (ZGA) genes. CG-poor R-loops inhibit DDX21 helicase activity on the 7SK/HEXIM1 snRNP complex, restricting CDK9 release and subsequent phosphorylation of Ser2 at the C-terminal domain of RNA polymerase II (RNAPII S2p) — the biochemical hallmark of pause release — thus enforcing RNAPII accumulation at major ZGA gene promoters to ensure productive transcription. These findings establish R-loops as direct modulators of RNAPII pause release, promoting the temporal fidelity of gene expression during the MZT.
{"title":"R-loops orchestrate RNAPII transcriptional reprogramming for the maternal-to-zygotic transition","authors":"Yaoyi Li, Qing Li, Xinxiu Wang, Chao Di, Yingliang Sheng, Ying Ma, Junzhi Liao, Qingqing Cai, Sainan Huang, Jiayu Chen, Guangming Wu, Lingling Zhang, Guangjin Pan, Shaorong Gao, Hongjie Yao","doi":"10.1038/s41422-025-01208-2","DOIUrl":"10.1038/s41422-025-01208-2","url":null,"abstract":"R-loops are pervasive genomic structures that link epigenetic modification and transcriptional regulation. However, the functional roles and regulatory mechanisms of R-loops during preimplantation development in mammals remain unexplored. Here, we reveal that the reprogramming of R-loops across developmental stages depends on CG density, with CG-poor R-loops more stage specific and strongly associated with early embryonic development. Loss of CG-poor R-loops causes severe defects in the maternal-to-zygotic transition (MZT) and preimplantation embryo development. This abnormal maintenance of CG-poor R-loops promotes premature activation of major zygotic genome activation (ZGA) genes. CG-poor R-loops inhibit DDX21 helicase activity on the 7SK/HEXIM1 snRNP complex, restricting CDK9 release and subsequent phosphorylation of Ser2 at the C-terminal domain of RNA polymerase II (RNAPII S2p) — the biochemical hallmark of pause release — thus enforcing RNAPII accumulation at major ZGA gene promoters to ensure productive transcription. These findings establish R-loops as direct modulators of RNAPII pause release, promoting the temporal fidelity of gene expression during the MZT.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"36 3","pages":"181-196"},"PeriodicalIF":25.9,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145919920","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}
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