EMBO Journal最新文献

Comprehensive proteomic profiling reveals mRNA splicing suppression during human oocyte aging.

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-02 DOI: 10.1038/s44318-026-00921-x

Changjian Yin, Zhenzhen Hou, Rusong Zhao, Miaomiao Wang, Shengjie Ling, Chuanxin Zhang, Xiaoou Feng, Shigang Zhao, Zi-Jiang Chen, Keliang Wu, Honghui Zhang, Xuejiang Guo, Han Zhao

{"title":"Comprehensive proteomic profiling reveals mRNA splicing suppression during human oocyte aging.","authors":"Changjian Yin, Zhenzhen Hou, Rusong Zhao, Miaomiao Wang, Shengjie Ling, Chuanxin Zhang, Xiaoou Feng, Shigang Zhao, Zi-Jiang Chen, Keliang Wu, Honghui Zhang, Xuejiang Guo, Han Zhao","doi":"10.1038/s44318-026-00921-x","DOIUrl":"https://doi.org/10.1038/s44318-026-00921-x","url":null,"abstract":"Reproductive aging impairs female fertility, and oocyte aging is considered a major driver of this phenotype, which manifests with increased aneuploidy and miscarriage risk, while no effective treatments have been widely implemented to date. Here, we report comprehensive protein expression profiling of oocytes during human aging, comparing fully grown germinal vesicle oocytes (FGO) and metaphase II (MII) oocytes; we describe the effect of aging on the maturation profiles across multiple age groups, including 25, 30, 35, and 40 years old. This analysis uncovered differential protein dynamics upon aging, with FGOs displaying protein expression alterations as early as 30 years, whereas these changes were delayed until the age of 35 or 40 in MII oocytes, particularly in proteins associated with mRNA splicing, translation, and chromosome segregation. Integration with transcriptomic data revealed suppression of splicing machineries as a potential initiating factor driving oocyte aging, characterized by deficiencies in mitochondrial function and chromosome segregation. This was validated by splicing inhibition, which suppressed mitochondrial function and ROS levels in mouse and human oocytes. Further, splicing factor DHX15 was identified as a candidate regulator of stage-specific oocyte aging. Together, our work systematically delineates the dynamic protein landscapes of human oocytes across multiple age groups, providing molecular targets and potential therapeutic strategies for clinical intervention.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327151","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}

引用次数: 0

Safe lysosomal sequestration of ferrous iron is mediated via cholesterol shielding and drives senescence and ferroptosis resistance.

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-02 DOI: 10.1038/s44318-026-00939-1

Izumi Yanatori, Tasuku Hirayama, Raku Son, Yasuhiro Murakawa, Yuta Matsuoka, Yuki Sugiura, Masato Niwa, Tatsuya Katsuno, Masahiko Tsujimoto, Hiroyuki Yasui, Atsuyasu Sato, Makoto Nakanishi, Kazuhiro Iwai

{"title":"Safe lysosomal sequestration of ferrous iron is mediated via cholesterol shielding and drives senescence and ferroptosis resistance.","authors":"Izumi Yanatori, Tasuku Hirayama, Raku Son, Yasuhiro Murakawa, Yuta Matsuoka, Yuki Sugiura, Masato Niwa, Tatsuya Katsuno, Masahiko Tsujimoto, Hiroyuki Yasui, Atsuyasu Sato, Makoto Nakanishi, Kazuhiro Iwai","doi":"10.1038/s44318-026-00939-1","DOIUrl":"https://doi.org/10.1038/s44318-026-00939-1","url":null,"abstract":"Iron accumulation is a conserved hallmark of cellular as well as organismal aging, yet its mechanistic role in senescence remains largely elusive. Here we show that the accumulation of ferrous iron (Fe2+) in lysosomes, a unique feature of senescent cells, is crucial for the induction of multiple senescence-associated phenotypes. Intriguingly, we found that this lysosomal Fe2+ sequestration is rendered \"safe\" by a dual metabolic adaptation that confers robust resistance to ferroptosis. First, Fe2+ accumulation triggers lysosomal alkalinization and subsequent cholesterol accumulation, which reinforces the lysosomal membrane against permeabilization. Second, senescent cells partition polyunsaturated fatty acids into lipid droplets, thereby depleting these ferroptosis-prone substrates from cellular membranes. Our findings establish that such cholesterol-enabled safe sequestration of Fe2+ serves as a central modulator linking senescence-associated remodeling to ferroptosis resistance. Modulating this lysosomal iron-centered pathway may provide new opportunities to target and control the behavior of senescent cells.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327152","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}

引用次数: 0

CDC7 and CDK8 kinases cooperate to support DNA replication origin firing in human cells.

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-02 DOI: 10.1038/s44318-026-00930-w

Michael D Rainey, Stefanus Bernard, Aikaterini Pravi, Liadhan Farrell, Yeray Hernández-Reyes, Aline M Morrison, Dominik Boos, Colm J Ryan, Corrado Santocanale

{"title":"CDC7 and CDK8 kinases cooperate to support DNA replication origin firing in human cells.","authors":"Michael D Rainey, Stefanus Bernard, Aikaterini Pravi, Liadhan Farrell, Yeray Hernández-Reyes, Aline M Morrison, Dominik Boos, Colm J Ryan, Corrado Santocanale","doi":"10.1038/s44318-026-00930-w","DOIUrl":"https://doi.org/10.1038/s44318-026-00930-w","url":null,"abstract":"The coordinated activation of DNA replication origins is important for efficient DNA synthesis and genome stability. S-phase cyclin-dependent kinases (CDKs), together with CDC7 kinase, are essential for origin activation by converting the pre-replicative complex into a fully active helicase. Here, in order to identify genes that tune DNA replication, we performed a chemogenetic genome-wide CRISPR-KO screen in cells challenged with the CDC7 inhibitor XL413. By developing a methodology based on genetic co-essentiality to functionally cluster the hits, we uncover the transcriptional CDK8/CCNC kinase in a cluster with replication initiation factors. Depletion of CDK8 further reduces the rate of DNA synthesis imposed by CDC7 inhibitors. DNA fibre experiments further support that CDK8 and CDC7 cooperate in origin activation. Suppression of DNA synthesis by CDK8 inhibition requires the binding of CDK8/CCNC to the MDM2 Binding Protein (MTBP), and we show that CDC7 and CDK8 associate with the MCM complex and individually contribute to the phosphorylation of the replicative helicase. In conclusion, this work adds CDK8 to the list of kinases directly involved in origin activation in human cells.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327150","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}

引用次数: 0

MCM10 and SLD-2/RECQL4 jointly activate the CMG helicase during metazoan DNA replication initiation. MCM10和SLD-2/RECQL4在后生动物DNA复制起始过程中共同激活CMG解旋酶。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-01 Epub Date: 2026-09-28 DOI: 10.1038/s44318-026-00915-9

Remi Sonneville, Cecile Evrin, Jane Wright, He Huang, Yisui Xia, Karim P M Labib

{"title":"MCM10 and SLD-2/RECQL4 jointly activate the CMG helicase during metazoan DNA replication initiation.","authors":"Remi Sonneville, Cecile Evrin, Jane Wright, He Huang, Yisui Xia, Karim P M Labib","doi":"10.1038/s44318-026-00915-9","DOIUrl":"10.1038/s44318-026-00915-9","url":null,"abstract":"Eukaryotic cells regulate the assembly and activation of the essential DNA helicase at the heart of the chromosome replication machinery, to ensure that the chromosomes are copied just once per cell cycle. The Mcm10 protein is essential for helicase activation in budding yeast, but an equivalent role for MCM10 orthologues in animal cells has not been explored. Moreover, complete deletion of the mcm-10 gene is viable in the nematode Caenorhabditis elegans, suggesting the involvement of additional factors. Here we show that MCM-10 and a second factor called SLD-2 are recruited to chromatin after helicase assembly in the C. elegans early embryo and are partially redundant for helicase activation. Moreover, deletion of the Mcm10 gene is viable in mouse embryonic stem cells, but causes synthetic lethality in the absence of RECQL4, which is the orthologue of SLD-2 in vertebrate species. Helicase activation is blocked in the combined absence of MCM10 and RECQL4, mirroring the situation in C. elegans. These findings indicate that metazoan helicase activation requires two conserved factors that are mutated in human disease.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"7582-7620"},"PeriodicalIF":8.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076649","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}

引用次数: 0

A functional screen for bacterial ubiquitin regulation identifies an unusual Pseudomonas aeruginosa E3 ligase. 细菌泛素调节的功能筛选确定了一个不寻常的铜绿假单胞菌E3连接酶。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-01 Epub Date: 2026-09-28 DOI: 10.1038/s44318-026-00917-7

Cameron G Roberts, Supender Kaur, Shun-Je Bhark, Aaron J Ogden, Michael E Divine, Gus D Warren, Donghoon Kang, Natalia V Kirienko, Paul P Geurink, Monique P C Mulder, Ernesto S Nakayasu, Jason E McDermott, Joshua N Adkins, Alejandro Aballay, Jonathan N Pruneda

{"title":"A functional screen for bacterial ubiquitin regulation identifies an unusual Pseudomonas aeruginosa E3 ligase.","authors":"Cameron G Roberts, Supender Kaur, Shun-Je Bhark, Aaron J Ogden, Michael E Divine, Gus D Warren, Donghoon Kang, Natalia V Kirienko, Paul P Geurink, Monique P C Mulder, Ernesto S Nakayasu, Jason E McDermott, Joshua N Adkins, Alejandro Aballay, Jonathan N Pruneda","doi":"10.1038/s44318-026-00917-7","DOIUrl":"10.1038/s44318-026-00917-7","url":null,"abstract":"Bacterial pathogens have adapted secreted effector proteins that hijack host ubiquitination to gain control over host responses. These effectors can exhibit, for example, E3 ligase or deubiquitinase activities, often without any homology to eukaryotic regulators. Such convergence in function poses a challenge to the discovery of additional ubiquitin-targeted virulence factors. Pseudomonas aeruginosa, for example, is a pervasive opportunistic pathogen with numerous mechanisms of virulence, yet no described E3 ligases or deubiquitinases. We have developed a workflow to functionally screen natively secreted bacterial effectors for ubiquitin regulatory activities. After benchmarking this approach on Salmonella Typhimurium, Enteropathogenic Escherichia coli, and Shigella flexneri, we identified a cryptic E3 ligase secreted by P. aeruginosa, which we have termed Pseudomonas Ub ligase 1 (PUL-1). PUL-1 resembles none of the other E3 ligases previously established in or outside of the eukaryotic system. Importantly, in an animal model of P. aeruginosa infection, PUL-1 ligase activity plays an important role in regulating virulence. Thus, functional identification of ubiquitin-targeted effectors can expand our appreciation of ubiquitin regulation during bacterial pathogenesis.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"7489-7514"},"PeriodicalIF":8.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076568","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}

引用次数: 0

Dynamic control of cell state transitions during tissue morphogenesis. 组织形态发生过程中细胞状态转换的动态控制。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.1038/s44318-026-00905-x

Joana E Saraiva, Sandra Edwards-Jorquera, Elias H Barriga

引用次数: 0

Reciprocal coupling between EMT and BMP morphogen signalling drives collective cell invasion. EMT和BMP形态因子信号之间的相互耦合驱动集体细胞入侵。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1038/s44318-026-00916-8

Yuri Takahashi, Alexandra Neaverson, Lara Busby, Filip Twarowski, Carlos Camacho-Macorra, Guillermo Serrano Nájera, Benjamin Steventon

{"title":"Reciprocal coupling between EMT and BMP morphogen signalling drives collective cell invasion.","authors":"Yuri Takahashi, Alexandra Neaverson, Lara Busby, Filip Twarowski, Carlos Camacho-Macorra, Guillermo Serrano Nájera, Benjamin Steventon","doi":"10.1038/s44318-026-00916-8","DOIUrl":"10.1038/s44318-026-00916-8","url":null,"abstract":"During collective cell invasion, epithelial-to-mesenchymal transition (EMT) and morphogen signalling-mediated cell fate specification are traditionally viewed as a linear cascade: morphogens drive cell fates that activate EMT gene expression programs. Here, we uncover reciprocal coupling between EMT initiation and BMP signalling mediated by SNAI2 and SMAD1. Using ex vivo chick tissue explants, we demonstrate that substrate-induced migration upregulates SMAD1 expression, activating BMP signalling across germ layers. Single-cell RNA sequencing reveals SNAI2 and SMAD1 co-expression in EMT initiation regions, and SNAI2 overexpression is sufficient to induce ectopic SMAD1 expression in vivo. Ex vivo CRISPR-Cas9 experiments further demonstrate that SNAI2 is required for SMAD1 expression and BMP signalling. While BMP signalling is dispensable for EMT initiation, it regulates cell fate proportions, dispersal dynamics, precursor region depletion rates, and migration directionality. This coupling provides a mechanism for synchronising cell fate specification with invasion progression during axis elongation, positioning SNAI2-SMAD1 interaction as mechanism to coordinate cell fate specification and EMT during collective cell invasion.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"7347-7373"},"PeriodicalIF":8.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128499","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}

引用次数: 0

In-situ cryo-ET of mouse embryos reveals cytoplasmic lattices contain ubiquitin-charged E2-E3 ligase assemblies. 小鼠胚胎的原位冷冻et显示细胞质晶格中含有带泛素的E2-E3连接酶组合。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-11-01 Epub Date: 2026-08-10 DOI: 10.1038/s44318-026-00895-w

Kashish Singh, Katarina Harasimov, Kathy K Niakan, Andrew P Carter

{"title":"In-situ cryo-ET of mouse embryos reveals cytoplasmic lattices contain ubiquitin-charged E2-E3 ligase assemblies.","authors":"Kashish Singh, Katarina Harasimov, Kathy K Niakan, Andrew P Carter","doi":"10.1038/s44318-026-00895-w","DOIUrl":"10.1038/s44318-026-00895-w","url":null,"abstract":"Cytoplasmic lattices (CPLs) are filamentous assemblies essential for mammalian embryonic development. They are known to regulate organelle organization, spindle assembly, and protein homeostasis, but their molecular functions remain unclear. Here, we develop a strategy combining cryo-focused ion beam milling and cryo-electron tomography to resolve macromolecular complexes directly in mammalian embryos. Using this approach, we determine the in situ structure of cytoplasmic lattices within 6/8-cell mouse embryos at ~4.7 Å resolution. CPL filaments are built from multiple copies of at least fourteen proteins arranged into a ~4.5 MDa repeating unit. The repeat contains a central cavity that is open at the back and lined with multiple FBXW-SKP1 complexes and three modules, each containing the E2 ubiquitin-conjugating enzyme UBE2D and the E3 ligase UHRF1. We resolve two CPL states: one is consistent with a ubiquitin-charged UBE2D, where ubiquitin is held in an open, inactive conformation by binding the scaffold protein PADI6; the second lacks discernible ubiquitin density and shows structural changes compatible with ubiquitin becoming available for transfer. Our findings support a model in which CPLs function as large ubiquitin ligase assemblies during early embryonic development.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":"7405-7437"},"PeriodicalIF":8.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708287","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}

引用次数: 0

ATAD2B governs epigenetic silencing of the epithelial program to fuel cancer metastasis and neuronal migration. ATAD2B调控上皮程序的表观遗传沉默，从而促进癌症转移和神经元迁移。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-10-30 DOI: 10.1038/s44318-026-00933-7

Arun Mahesh, Mohammed Inayatullah, Mikkel G Terp, Ziyi Zang, Charles Mariasoosai, Martin R Larsen, Carla Maria L Alves, Odd L Gammelgaard, Henrik J Ditzel, Vijay K Tiwari

{"title":"ATAD2B governs epigenetic silencing of the epithelial program to fuel cancer metastasis and neuronal migration.","authors":"Arun Mahesh, Mohammed Inayatullah, Mikkel G Terp, Ziyi Zang, Charles Mariasoosai, Martin R Larsen, Carla Maria L Alves, Odd L Gammelgaard, Henrik J Ditzel, Vijay K Tiwari","doi":"10.1038/s44318-026-00933-7","DOIUrl":"https://doi.org/10.1038/s44318-026-00933-7","url":null,"abstract":"Epithelial-to-mesenchymal transition (EMT) is a pivotal developmental program that is frequently co-opted to drive cancer aggressiveness and metastasis. While the dynamic remodelling of histone H3 lysine 27 acetylation (H3K27ac) landscapes is a hallmark of EMT, the specific chromatin readers decoding these epigenetic signals remain largely unknown. Here, we identify ATAD2B as a novel H3K27ac reader essential for cell migration in both cancer metastasis and brain development. Multi-omics profiling revealed that, at EMT onset, ATAD2B targets H3K27ac at active epithelial identity genes via its bromodomain and recruits HDAC1 to epigenetically silence them, enforcing a mesenchymal state. ATAD2B loss impairs migration and invasion in breast cancer lines and Patient-Derived organoids, whereas its overexpression accelerates in vivo lung metastasis and correlates with poor patient survival. Furthermore, ATAD2B promotes the migration of newborn neurons in the developing brain. Our findings establish ATAD2B as a versatile chromatin reader orchestrating cell motility across development and disease.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301938","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}

引用次数: 0

Cis-regulatory co-option of a transposon family reinforces cell identity across the immune system. 转座子家族的顺式调控共选择增强了免疫系统中的细胞身份。

IF 8.4 1区生物学

EMBO Journal Pub Date : 2026-10-28 DOI: 10.1038/s44318-026-00938-2

Jason D Chobirko, Cédric Feschotte, Andrew Grimson

{"title":"Cis-regulatory co-option of a transposon family reinforces cell identity across the immune system.","authors":"Jason D Chobirko, Cédric Feschotte, Andrew Grimson","doi":"10.1038/s44318-026-00938-2","DOIUrl":"10.1038/s44318-026-00938-2","url":null,"abstract":"Transposable elements (TEs) comprise about half of the human and mouse genomes and contribute to gene regulation during immune responses. However, how TEs acquire cis-regulatory functions during immune cell development remains poorly understood. Here, we analyzed hundreds of datasets profiling chromatin accessibility, gene expression, transcription factor occupancy and DNA-DNA contact across diverse mouse and human immune cell types. We identified two rodent-specific TE subfamilies, ORR1E and ORR1D2 (collectively, ODE) that have diversified after genomic insertion into cell type-specific enhancers across the mouse immune system. Post-insertion mutations in ODE loci generated differential binding sites for lineage-specifying transcription factors. ODEs showed evidence of evolutionary sequence constraint and contacted promoters of hundreds of genes in immune cells. Predicted ODE target genes were enriched for cell type-specific functions and showed increased expression in mouse compared to human cell types lacking ODEs. Together, these findings show how a single TE family can diversify after genomic spread to generate cell type-specific enhancers that reinforce lineage-specific gene programs.","PeriodicalId":50533,"journal":{"name":"EMBO Journal","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149301930","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}

引用次数: 0