Cell Death and Differentiation最新文献

{"title":"Inverse and dynamic levels of H3K4me3 and H3K27me3 regulate mouse postnatal dental gyrus development","authors":"Yan Luan, Hanyue Zhang, Yingfei Liu, Jing Zhou, Wen Li, Kaige Ma, Xiaoyan Zheng, Chen Huang, Xinlin Chen, Haixia Lu, Hui Yu, Magnar Bjørås, Arne Klungland, Zhichao Zhang","doi":"10.1038/s41418-025-01563-y","DOIUrl":"https://doi.org/10.1038/s41418-025-01563-y","url":null,"abstract":"<p>The dentate gyrus (DG), a crucial region of the hippocampus responsible for learning, spatial encoding, and memory formation, undergoes its main development and maturation after birth. Despite its importance, the regulatory mechanisms underlying postnatal DG development remain poorly understood. This study is aimed to investigate the role of H3 lysine 4 trimethylation (H3K4me3) and H3 lysine 27 trimethylation (H3K27me3) in the development and function of the postnatal DG. We show robust enrichment of H3K4me3 in the subgranular zone (SGZ), a primary neurogenic region, while high levels of H3K27me3 were mainly presented in granule cell layer. Enhanced H3K4me3 level facilitated proliferation and development of neonatal mouse neural stem cells (NSCs), promoted differentiation towards GABA neurons, as well as improved mouse spatial learning and memory. Enhancing H3K27me3 level exerts the opposite function, additionally promoting NSCs entry into a quiescent-like state. During the neuronal differentiation of NSCs, the integration of RNA-Seq and ChIP-Seq datasets reveals that H3K4me3 and H3K27me3 co-regulate the expression of genes essential for neural development, such as Gli1, through the formation of bivalent domains. Manipulation activation of the Shh/Gli1 pathway abolishes the effect of alterations in the levels of H3K4me3 and H3K27me3 in NSCs. Based on these findings, we propose that H3K4me3 and H3K27me3 serve as molecular “switches” to dynamically regulate NSCs proliferation and differentiation and in turn, influence the postnatal developmental progression of DG, additionally to provide potential therapeutic targets for treating diseases associated with abnormal hippocampal development.</p><figure><p>During dentate gyrus development in neonatal mice, the active transcription mark H3K4me3 and the repressive mark H3K27me3 are co-localized at the promoter regions of essential neurodevelopmental genes, and thus forming bivalent chromatin domains in neural stem cells. These domains serve as a “molecular switch” that regulates the dynamic processes of cell proliferation and differentiation. The enhanced ratio of H3K4me3 to H3K27me3 markedly upregulates the expression related genes, thereby promoting cell proliferation and neuronal differentiation, ultimately leading to improved spatial learning and memory. Conversely, decreasing this ratio has the opposite effect.</p></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"18 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900557","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":"BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM","authors":"Marianne Quaas, Robin Kohler, Lukas Nöltner, Louisa F. Schmidbauer, Sigrid Uxa, Gerd A. Müller, Kurt Engeland","doi":"10.1038/s41418-025-01566-9","DOIUrl":"https://doi.org/10.1038/s41418-025-01566-9","url":null,"abstract":"<p>BRCA1 and BRCA2 proteins are crucial for DNA repair through homologous recombination (HR), which predominantly takes place during S and G₂ phases. Their expression is tightly regulated to ensure HR occurs exclusively within these phases. While these proteins are well-established tumor suppressors in hereditary breast and ovarian cancers, their inactivation is rare across all sporadic cancers. Counterintuitively, BRCA1 and BRCA2 expression is downregulated rather than upregulated following DNA damage and p53 activation. In this study, we demonstrate that <i>BRCA1</i> and <i>BRCA2</i> gene expression is governed by the same transcriptional mechanisms throughout the cell cycle, peaking in the S phase. During G₀/G₁ and following p53 activation, <i>BRCA1/2</i> transcription is repressed by DREAM and RB:E2F repressor complexes. Importantly, this transcriptional repression occurs concurrently with the coordinated downregulation of numerous genes involved in cell cycle control and DNA repair pathways. Consistent with previous findings, this suppression notably affects members of the Fanconi anemia group and is mediated through the DREAM complex. Such broad transcriptional suppression facilitates exit from S phase, thereby promoting a fundamental shift in DNA repair mechanisms. Following DNA damage, we demonstrate that <i>BRCA1/2</i> downregulation occurs indirectly through the p53-p21-DREAM/RB axis, wherein p53-induced <i>p21/CDKN1A</i> expression initiates repression dependent on DREAM and RB. These results, together with observations from previous studies, suggest that DNA repair shifts from HR to the error-prone pathways of non-homologous end joining (NHEJ) and single-strand annealing (SSA), resulting in chromosomal aberrations and cell death, thereby in fact preventing malignant transformation. Our findings elucidate the transcriptional regulation of <i>BRCA1</i> and <i>BRCA2</i> expression. These regulatory mechanisms, when considered alongside prior findings and hypotheses, may help explain why BRCA1 and BRCA2 proteins do not exhibit tumor-suppressive functions in most cell types.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"3 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900558","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":"PUMA-induced apoptosis drives bone marrow failure and genomic instability in telomerase-deficient mice.","authors":"Christian Molnar, Jovana Rajak, Julia Miriam Weiss, Irene Gonzalez-Menendez, Geoffroy Andrieux, Franziska Schreiber, Eva-Maria Kornemann, Lena Wendeburg, Gudrun Göhring, Brigitte Strahm, Fabian Beier, Doris Steinemann, Melanie Börries, Martina Rudelius, Leticia Quintanilla-Martinez, Charlotte M Niemeyer, Marena R Niewisch, Verena Labi, Sheila Bohler, Miriam Erlacher","doi":"10.1038/s41418-025-01557-w","DOIUrl":"10.1038/s41418-025-01557-w","url":null,"abstract":"<p><p>Bone marrow failure is a severe complication of human telomere biology disorders and predisposes individuals to secondary leukemia. A deeper understanding of this process could offer significant clinical benefits. Using a preclinical mouse model deficient in the RNA component of the telomerase (mTerc), we demonstrate that bone marrow failure results from excessive apoptosis, predominantly mediated by the pro-apoptotic p53 target PUMA. Genetic ablation of Puma alleviates hematological phenotypes and reduces the risk of lethal bone marrow failure while preserving genomic stability. Mechanistically, PUMA deficiency decreases the sensitivity of hematopoietic cells to lethal stressors, including critically short telomeres. As a consequence, reduced compensatory turnover of hematopoietic progenitors slows down telomere shortening at the population level, delays stem cell exhaustion, and diminishes the acquisition of somatic mutations - ultimately preventing neoplastic transformation. Elevated expression of both p53 and PUMA is also observed in the bone marrow from patients with telomere biology disorders. While apoptosis resistance is traditionally associated with malignant transformation, our findings provide evidence that selective inhibition of PUMA-mediated apoptosis may represent a viable therapeutic strategy to prevent or delay leukemic transformation in this patient population.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":15.4,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882293","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":"Intestinal metabolite TMAO promotes CKD progression by stimulating macrophage M2 polarization through histone H4 lysine 12 lactylation.","authors":"Youzhou Tang, Yuxin Li, Xinyu Yang, Tianze Lu, Xinran Wang, Zhi Li, Jun Liu, Jianwen Wang","doi":"10.1038/s41418-025-01554-z","DOIUrl":"10.1038/s41418-025-01554-z","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) progression is tightly associated with renal fibrosis, which is regulated by macrophage M2 polarization. The intestinal metabolite trimethylamine N-oxide (TMAO) has been reported to promote CKD, yet its underlying mechanism remains unclear. Here, we elucidated a mechanism wherein TMAO excreted through the kidneys alters the pyruvate metabolism of renal tubular epithelial cells, resulting in the production of lactic acid. Local lactic acid accumulation in the kidney promotes adjacent macrophage M2 polarization, a process speculated to be mediated by specific lactylation of macrophage genes. Through lactylation omics analysis, we identified histone H4 lysine 12 (H4K12) as the most significantly up-regulated lysine residue subjected to lactylation. Subsequent chromatin immunoprecipitation sequencing (ChIP-seq) assays revealed H4K12 lactylation on several glycometabolism gene promoters and genes. Furthermore, we found that this lactylation-mediated epigenetic regulation requires the assistance of the \"porter\"protein p300, as knockdown of p300 weakened the trend towards M2 polarization induced by lactic acid. Using an in vivo unilateral ureteral obstruction (UUO) mouse model, we verified the M2 polarization effect of TMAO and its detrimental role in CKD, as well as the protective effect of the TMAO inhibitor iodomethylcholine (IMC) on CKD. Clinical data validated the up-regulated TMAO's effect on renal M2 polarization and fibrosis. Our findings suggest that CKD patients exhibit increased TMAO levels, which modulate the production of lactic acid by renal intrinsic cells. Epigenetic regulations mediated by lactic acid, particularly H4K12la on macrophage genes involved in glycometabolism, may contribute to M2 polarization. Targeting TMAO or its downstream pathways could have potential therapeutic benefits in CKD. Schematic diagram showing the whole TMAO modulation process. CKD dysfunction of microbiota leads to elevated TMA. TMA metabolized through liver into TMAO which excreted 90% through kidney. Renal tubular epithelial cells contact with TMAO and secrete lactic acid affecting adjacent macrophages more into M2 type through gene histone H4K12la under the help of p300 as a carrier. These genes include a large amount of glucose metabolism related genes which could at least partially explain this M2 polarization.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":15.4,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882292","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":"TRIM32 promotes anoikis resistance and metastasis in NSCLC by degrading CHEK2 to enhance IL-6 secretion.","authors":"Jia Xu, Wenjun Liu, Li Chen, Juan Zhang, Dongze Zhang, Xue Huang, Guangbo Zhang","doi":"10.1038/s41418-025-01559-8","DOIUrl":"10.1038/s41418-025-01559-8","url":null,"abstract":"<p><p>Metastasis significantly contributes to the high mortality of non-small cell lung cancer (NSCLC), with anoikis resistance playing a critical role in this process. However, the role of TRIM32 in anoikis resistance and metastasis is not well understood. In this study, we demonstrate that TRIM32 enhances both anoikis resistance and metastasis in NSCLC. We confirmed the interaction between TRIM32 and CHEK2, and showed that TRIM32 mediates the degradation of CHEK2 via K48-linked polyubiquitination. Our results indicate that CHEK2 suppresses anoikis resistance and metastasis in NSCLC, both in vitro and in vivo. Additionally, we found that TRIM32 upregulates IL-6 expression, an effect that is reversed by the overexpression of CHEK2. Further analysis confirmed that IL-6 plays a key role in TRIM32-mediated anoikis resistance and metastasis. Notably, TRIM32⁺CHEK2^-IL-6⁺ tumor cells were more prevalent in NSCLC tissues with lymph node metastasis. In conclusion, our findings suggest that targeting TRIM32 to inhibit anoikis resistance and metastasis, via the CHEK2/IL-6 axis, may provide a novel therapeutic strategy for treating metastatic NSCLC. The mechanisms by which TRIM32 promotes anoikis resistance and metastasis in NSCLC. Schematic diagram showing the regulatory mechanisms of TRIM32 promotes anoikis resistance and metastasis in NSCLC by degrading CHEK2 to promote IL-6 secretion.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":15.4,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871680","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":"The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagy","authors":"Peihua Zhang, Keping Feng, Xiao Yu, Yi Yang, Siyu Luo, Qiao Li, Hailong Zhang, Yachun Jia, Qiaoman Fei, Xiaomin Ren, Hongwei Liu, Lin Li, Dan Yang, Gustave Munyurangabo, Jingze Yue, Qian Li, Pengyu Zhang, Lingqin Song, Aili He, Zhanping Lu, Linlin Zhang, Guangyao Kong","doi":"10.1038/s41418-025-01561-0","DOIUrl":"https://doi.org/10.1038/s41418-025-01561-0","url":null,"abstract":"<p>The N6-methyladenosine (m6A) modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutation-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase methyltransferase-like 14 (METTL14) was highly expressed and associated with a shorter survival in a RAS-mutation myeloid malignancy, juvenile myelomonocytic leukemia (JMML). The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a <i>Kras</i>^{<i>G12D/+</i>} mutation-induced mouse model of JMML. Moreover, knockout of METTL14 reduces hyperproliferation of <i>Kras</i>^{<i>G12D/+</i>} HSPCs and suppresses oncogenic <i>Kras</i>^{<i>G12D/+</i>}-induced myeloid disease in a cell-autonomous manner. Mechanistically, we revealed that the knockout of METTL14 reduced the autophagy levels of HSPCs by suppressing the transcription and translation of autophagy-related genes, such as autophagy-related gene 5 (<i>Atg5</i>) and autophagy-related gene 9 (<i>Atg9a</i>), through m6A modification. Furthermore, we found that the autophagy inhibition through knockout of ATG5 in <i>Kras</i>^{<i>G12D/+</i>} mutant mice promoted the expansion of HSPCs and inhibited the progression of leukemia disease, consistent with the phenotypes of knockout of METTL14. Finally, we observed that combined treatment with a m6A inhibitor and a MEK inhibitor synergistically suppressed JMML growth. Collectively, these findings highlight the critical role of METTL14 in JMML tumorigenesis and suggest that m6A modification represents a promising therapeutic target for this disease.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"21 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860085","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 positive feedback loop between SERPINH1 and MMP-9/TGF-β1 promotes lung adenocarcinoma progression","authors":"Yang Zhou, Xueying Wang, Hongyan Li, Menglin Fan, Minghao Wang, Weitong Gao, Zhihao Shi, Jiale Wang, Jiaqi Tan, Fang Liu","doi":"10.1038/s41418-025-01558-9","DOIUrl":"https://doi.org/10.1038/s41418-025-01558-9","url":null,"abstract":"<p>Lung adenocarcinoma (LUAD), the most predominant subtype of lung cancer, is a leading cause of cancer-related death worldwide. However, its underlying molecular mechanisms remain poorly understood. In this study, we identified that SERPINH1, a member of the serine protease inhibitor (serpin) superfamily, is upregulated in LUAD tissues and cells. Furthermore, high expression of SERPINH1 is associated with poor prognosis in patients. Functional experiments revealed that overexpression of SERPINH1 promotes the proliferation, invasion, and migration of LUAD cells. Further investigation showed that MMP-9 is a novel binding partner of SERPINH1. SERPINH1 enhances the protein levels of MMP-9 by inhibiting its ubiquitination, which in turn promotes the activation and secretion of extracellular TGF-β1, leading to the activation of cancer-associated fibroblasts (CAFs). Additionally, the sustained activation of TGF-β signaling further enhances the transcription of SERPINH1, establishing a positive feedback loop between SERPINH1 and TGF-β1. Taken together, our findings suggest that the SERPINH1/TGF-β1 positive feedback loop plays a crucial role in the onset and metastasis of LUAD. SERPINH1 may serve as a potential prognostic and therapeutic target in LUAD.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"182 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860110","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":"Reversible ALKBH5 cytosolic aggregation accelerates cellular senescence","authors":"Liqian Chen, Zixin Chen, Jiahui Mo, Qingqiang Xie, Wenjie Lin, Huiling Zheng, Yuxiu Zou, Yufan Chen, Xiu-Wu Bian, Zhongjun Zhou, Guoxiang Jin","doi":"10.1038/s41418-025-01560-1","DOIUrl":"https://doi.org/10.1038/s41418-025-01560-1","url":null,"abstract":"<p>Cellular senescence is the major hallmark and therapeutic target of aging and age-related diseases. The role of ALKBH5, one of the main m6A demethylases, in cellular senescence emerges however remains contentious. Herein, we show the reversible ALKBH5 aggregation in cytoplasm promotes cellular senescence. Mechanically, ALKBH5 aggregation causes cytosolic retention, resulting in the m6A dysregulation and m6A hypermethylation of <i>Cdk2</i>, which promotes <i>Cdk2</i> RNA instability to drive senescence. In addition, m6A imbalance aggravates ALKBH5 cytosolic aggregation in a feedback loop. We further demonstrate that ALKBH5 nuclear translocation required the formation of ALKBH5 droplet phase via binding Nucleoporin p62 (Nup62), while the aggregation of ALKBH5 traps with Nup62 in the cytoplasm. Reduced Nup62 prevents ALKBH5 nuclear entry leading to cellular senescence. Importantly, administration of m6A labeled RNA efficiently reverses ALKBH5 cytosolic aggregates and restores its nuclear entry to alleviate cellular senescence. Forced nuclear entry by NLS-ALKBH5 can prevent senescence in vitro and in vivo. Taken together, these findings unravel a novel paradigm for m6A epigenetic regulation in cellular senescence and offer promising therapeutic targets and strategies for the intervention of aging and age-associated diseases.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"134 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144851727","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":"ICAM-1 identifies preadipocytes and restricts white adipogenesis by adhering immune cells","authors":"Chunxing Zheng, Jiayin Ye, Qian Yang, Keli Liu, Cheng Chen, Jianchang Cao, Qing Li, Yueqing Xue, Hui Ma, Arnold B. Rabson, Changshun Shao, Fei Hua, Lydia Sorokin, Gerry Melino, Yufang Shi, Ying Wang","doi":"10.1038/s41418-025-01551-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01551-2","url":null,"abstract":"<p>Adipose stem cell hierarchy was delineated by scRNA-seq analysis, revealing that ICAM-1, a glycoprotein that mediates cell-cell interaction, is a preadipocyte marker. However, the cellular and molecular mechanisms of how ICAM-1⁺ preadipocytes contribute to adipose tissue homeostasis in vivo remain unclear. To address this, <i>Icam1</i>^{<i>+/CreERT2</i>} mice were generated, and it was demonstrated that ICAM-1-expressing progenitors actively participated in developing and remodeling white adipose tissue. Under a high-fat diet, both proliferation and adipogenic differentiation of ICAM-1⁺ preadipocytes increased significantly. Interestingly, ICAM-1 plays a critical role in maintaining the interaction between preadipocytes and immune cells, acting as a checkpoint on white adipogenesis. Mice lacking ICAM-1 specifically in stromal cells exhibited worsened hyperplastic obesity, showing heightened fatty acid synthesis and lipid storage in adipose tissue, and the related insulin resistance. In human adipose tissue, ICAM-1 also marked committed preadipocytes and mediated adhesion between preadipocytes and immune cells. Thus, our study shows that ICAM-1 marks preadipocytes and curbs adipogenesis by facilitating adhesion between preadipocytes and immune cells.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"12 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144851729","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":"Editorial Expression of Concern to: HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells.","authors":"P Peixoto, V Castronovo, N Matheus, C Polese, O Peulen, A Gonzalez, M Boxus, E Verdin, M Thiry, F Dequiedt, D Mottet","doi":"10.1038/s41418-025-01556-x","DOIUrl":"https://doi.org/10.1038/s41418-025-01556-x","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":15.4,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820678","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}