Cell Research最新文献_第10页

Author Correction: LKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate cancer 作者更正：LKB1失活促进前列腺癌表观遗传重塑诱导的谱系可塑性和抗雄激素耐药性

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-18 DOI: 10.1038/s41422-025-01097-5

Fei Li, Pengfei Dai, Huili Shi, Yajuan Zhang, Juan He, Anuradha Gopalan, Dan Li, Yu Chen, Yarui Du, Guoliang Xu, Weiwei Yang, Chao Liang, Dong Gao

引用次数: 0

SPO11 cuts!

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-17 DOI: 10.1038/s41422-025-01093-9

Sara Hariri, Neil Hunter

引用次数: 0

New insights into how parental worms protect their offspring 关于亲代蠕虫如何保护后代的新见解。

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-14 DOI: 10.1038/s41422-025-01094-8

Chenming Zeng, Eric A. Miska

引用次数: 0

Killing cancer quickly: inducing hyper-acute rejection of patient tumors 快速杀死癌症：诱导患者肿瘤的超急性排斥反应

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-13 DOI: 10.1038/s41422-025-01099-3

Eric Bartee

引用次数: 0

Publisher Correction: Comprehensive discovery and functional characterization of the noncanonical proteome 出版者更正：非典型蛋白质组的全面发现和功能表征

IF 28.1 1区生物学

Cell Research Pub Date : 2025-03-10 DOI: 10.1038/s41422-025-01091-x

Chengyu Shi, Fangzhou Liu, Xinwan Su, Zuozhen Yang, Ying Wang, Shanshan Xie, Shaofang Xie, Qiang Sun, Yu Chen, Lingjie Sang, Manman Tan, Linyu Zhu, Kai Lei, Junhong Li, Jiecheng Yang, Zerui Gao, Meng Yu, Xinyi Wang, Junfeng Wang, Jing Chen, Wei Zhuo, Zhaoyuan Fang, Jian Liu, Qingfeng Yan, Dante Neculai, Qiming Sun, Jianzhong Shao, Weiqiang Lin, Wei Liu, Jian Chen, Liangjing Wang, Yang Liu, Xu Li, Tianhua Zhou, Aifu Lin

引用次数: 0

Oncogenic RAS induces a distinctive form of non-canonical autophagy mediated by the P38-ULK1-PI4KB axis 致癌RAS诱导由P38-ULK1-PI4KB轴介导的独特形式的非规范自噬

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-07 DOI: 10.1038/s41422-025-01085-9

Xiaojuan Wang, Shulin Li, Shiyin Lin, Yaping Han, Tong Zhan, Zhiying Huang, Juanjuan Wang, Ying Li, Haiteng Deng, Min Zhang, Du Feng, Liang Ge

{"title":"Oncogenic RAS induces a distinctive form of non-canonical autophagy mediated by the P38-ULK1-PI4KB axis","authors":"Xiaojuan Wang, Shulin Li, Shiyin Lin, Yaping Han, Tong Zhan, Zhiying Huang, Juanjuan Wang, Ying Li, Haiteng Deng, Min Zhang, Du Feng, Liang Ge","doi":"10.1038/s41422-025-01085-9","DOIUrl":"10.1038/s41422-025-01085-9","url":null,"abstract":"Cancer cells with RAS mutations exhibit enhanced autophagy, essential for their proliferation and survival, making it a potential target for therapeutic intervention. However, the regulatory differences between RAS-induced autophagy and physiological autophagy remain poorly understood, complicating the development of cancer-specific anti-autophagy treatments. In this study, we identified a form of non-canonical autophagy induced by oncogenic KRAS expression, termed RAS-induced non-canonical autophagy via ATG8ylation (RINCAA). RINCAA involves distinct autophagic factors compared to those in starvation-induced autophagy and incorporates non-autophagic components, resulting in the formation of non-canonical autophagosomes with multivesicular/multilaminar structures labeled by ATG8 family proteins (e.g., LC3 and GABARAP). We have designated these structures as RAS-induced multivesicular/multilaminar bodies of ATG8ylation (RIMMBA). A notable feature of RINCAA is the substitution of the class III PI3K in canonical autophagy with PI4KB in RINCAA. We identified a regulatory P38-ULK1-PI4KB-WIPI2 signaling cascade governing this process, where ULK1 triggers PI4KB phosphorylation at S256 and T263, initiating PI4P production, ATG8ylation, and non-canonical autophagy. Importantly, elevated PI4KB phosphorylation at S256 and T263 was observed in RAS-mutated cancer cells and colorectal cancer specimens. Inhibition of PI4KB S256 and T263 phosphorylation led to a reduction in RINCAA activity and tumor growth in both xenograft and KPC models of pancreatic cancer, suggesting that targeting ULK1-mediated PI4KB phosphorylation could represent a promising therapeutic strategy for RAS-mutated cancers.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 6","pages":"399-422"},"PeriodicalIF":25.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41422-025-01085-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569557","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}

引用次数: 0

SETD1B-mediated broad H3K4me3 controls proper temporal patterns of gene expression critical for spermatid development setd1b介导的广泛H3K4me3控制对精子发育至关重要的基因表达的适当时间模式

IF 25.9 1区生物学

Cell Research Pub Date : 2025-03-04 DOI: 10.1038/s41422-025-01080-0

Zhen Lin, Bowen Rong, Ruitu Lyu, Yuxuan Zheng, Yao Chen, Junyi Yan, Meixia Wu, Xiaogang Gao, Fuchou Tang, Fei Lan, Ming-Han Tong

{"title":"SETD1B-mediated broad H3K4me3 controls proper temporal patterns of gene expression critical for spermatid development","authors":"Zhen Lin, Bowen Rong, Ruitu Lyu, Yuxuan Zheng, Yao Chen, Junyi Yan, Meixia Wu, Xiaogang Gao, Fuchou Tang, Fei Lan, Ming-Han Tong","doi":"10.1038/s41422-025-01080-0","DOIUrl":"10.1038/s41422-025-01080-0","url":null,"abstract":"Epigenetic programming governs cell fate determination during development through intricately controlling sequential gene activation and repression. Although H3K4me3 is widely recognized as a hallmark of gene activation, its role in modulating transcription output and timing within a continuously developing system remains poorly understood. In this study, we provide a detailed characterization of the epigenomic landscapes in developing male germ cells. We identified thousands of spermatid-specific broad H3K4me3 domains regulated by the SETD1B-RFX2 axis, representing a previously underappreciated form of H3K4me3. These domains, overlapping with H3K27ac-marked enhancers and promoters, play critical roles in orchestrating robust transcription and accurate temporal control of gene expression. Mechanistically, these broad H3K4me3 compete effectively with regular H3K4me3 for transcriptional machinery, thereby ensuring robust levels and precise timing of master gene expression in mouse spermiogenesis. Disruption of this mechanism compromises the accuracy of transcription dosage and timing, ultimately impairing spermiogenesis. Additionally, we unveil remarkable changes in the distribution of heterochromatin marks, including H3K27me3 and H3K9me2, during the mitosis-to-meiosis transition and completion of meiotic recombination, which closely correlates with gene silencing. This work underscores the highly orchestrated epigenetic regulation in spermatogenesis, highlighting the previously unrecognized role of Setd1b in the formation of broad H3K4me3 domains and transcriptional control, and provides an invaluable resource for future studies toward the elucidation of spermatogenesis.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 5","pages":"345-361"},"PeriodicalIF":25.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41422-025-01080-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538295","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}

引用次数: 0

NO-immune privilege for hematopoietic stem cells 造血干细胞无免疫特权。

IF 25.9 1区生物学

Cell Research Pub Date : 2025-02-28 DOI: 10.1038/s41422-025-01087-7

Agathe L. Chédeville, Simón Méndez-Ferrer

引用次数: 0

Structural insights into spliceosome fidelity: DHX35–GPATCH1- mediated rejection of aberrant splicing substrates 剪接体保真度的结构洞察：DHX35-GPATCH1介导的对异常剪接底物的排斥。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-02-28 DOI: 10.1038/s41422-025-01084-w

Yi Li, Paulina Fischer, Mengjiao Wang, Qianxing Zhou, Aixia Song, Rui Yuan, Wanyu Meng, Fei Xavier Chen, Reinhard Lührmann, Benjamin Lau, Ed Hurt, Jingdong Cheng

{"title":"Structural insights into spliceosome fidelity: DHX35–GPATCH1- mediated rejection of aberrant splicing substrates","authors":"Yi Li, Paulina Fischer, Mengjiao Wang, Qianxing Zhou, Aixia Song, Rui Yuan, Wanyu Meng, Fei Xavier Chen, Reinhard Lührmann, Benjamin Lau, Ed Hurt, Jingdong Cheng","doi":"10.1038/s41422-025-01084-w","DOIUrl":"10.1038/s41422-025-01084-w","url":null,"abstract":"The spliceosome, a highly dynamic macromolecular assembly, catalyzes the precise removal of introns from pre-mRNAs. Recent studies have provided comprehensive structural insights into the step-wise assembly, catalytic splicing and final disassembly of the spliceosome. However, the molecular details of how the spliceosome recognizes and rejects suboptimal splicing substrates remained unclear. Here, we show cryo-electron microscopy structures of spliceosomal quality control complexes from a thermophilic eukaryote, Chaetomium thermophilum. The spliceosomes, henceforth termed B*Q, are stalled at a catalytically activated state but prior to the first splicing reaction due to an aberrant 5’ splice site conformation. This state is recognized by G-patch protein GPATCH1, which is docked onto PRP8-EN and -RH domains and has recruited the cognate DHX35 helicase to its U2 snRNA substrate. In B*Q, DHX35 has dissociated the U2/branch site helix, while the disassembly helicase DHX15 is docked close to its U6 RNA 3’-end substrate. Our work thus provides mechanistic insights into the concerted action of two spliceosomal helicases in maintaining splicing fidelity by priming spliceosomes that are bound to aberrant splice substrates for disassembly.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 4","pages":"296-308"},"PeriodicalIF":28.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41422-025-01084-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522758","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}

引用次数: 0

Structural basis of phosphate export by human XPR1 人XPR1基因输出磷酸盐的结构基础。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-02-28 DOI: 10.1038/s41422-025-01081-z

Yifei Wang, Yuechan Wang, Hui Yang, Ao Li, Dan Ma, Huaizong Shen

引用次数: 0