Nucleic Acids Research最新文献_第5页

DHX36 modulates stress granule assembly independent of recruitment of mRNAs with G-quadruplex sequence motifs. DHX36调节胁迫颗粒组装独立于具有g -四重序列基序的mrna的募集。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf938

Li Yi Cheng,Nina Ripin,Thomas R Cech,Roy Parker

{"title":"DHX36 modulates stress granule assembly independent of recruitment of mRNAs with G-quadruplex sequence motifs.","authors":"Li Yi Cheng,Nina Ripin,Thomas R Cech,Roy Parker","doi":"10.1093/nar/gkaf938","DOIUrl":"https://doi.org/10.1093/nar/gkaf938","url":null,"abstract":"Stress granules are RNA-protein condensates that form in response to an increase in untranslating mRNPs (messenger ribonucleoproteins). Stress granules form by the condensation of mRNPs through a combination of protein-protein, protein-RNA, and RNA-RNA interactions. Several reports have suggested that G-rich RNA sequences capable of forming G-quadruplexes (rG4s) promote stress granule formation. Here, we provide three observations arguing that G-tracts do not promote messenger RNA (mRNA) accumulation in stress granules in human osteosarcoma cells. First, we observed no difference in the accumulation in stress granules of reporter mRNAs with and without G-tracts in their 3' UTRs. Second, in U-2 OS cell lines with reduced expression of DHX36, which is thought to unwind G-quadruplexes, the accumulation of endogenous mRNAs was independent of their predicted rG4-forming potential. Third, while mRNAs in stress granules initially appeared to have more rG4 motifs than bulk mRNAs, this effect disappeared when rG4 motif abundance was normalized to mRNA length. However, we observed that in a G3BP1/2 double knockout cell line, which strongly inhibits stress granule formation, reducing DHX36 expression rescued stress granule-like foci formation. This indicates that DHX36 can limit stress granule formation, potentially by unwinding trans-rG4s or limiting other intermolecular RNA-RNA interactions that promote stress granule formation.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"18 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145116684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Abundant bacterial nucleoid-associated protein H-NS limits plasmid transfer through mechanical modification of DNA. 丰富的细菌核相关蛋白H-NS限制了质粒通过DNA的机械修饰转移。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf928

Mingyue Fei,Mengdie Fang,Qi Zhou,Ziyan Chen,Mengxin Gong,Fabai Wu,Changfu Tian,Dongchang Sun

引用次数: 0

ATRX cooperates with TOP2B for replication fork stability and DNA damage response through G-quadruplex regulation. ATRX通过g -四重体调控与TOP2B共同参与复制叉稳定性和DNA损伤应答。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf939

Ying Pang,Meng Cheng,Jingzhe Wang,Rui Wang,Xu Chen,Chunyu Zhang,Yuntong Yang,Tongjie Ji,Min Liu,Jing Zhang,Chunlong Zhong

{"title":"ATRX cooperates with TOP2B for replication fork stability and DNA damage response through G-quadruplex regulation.","authors":"Ying Pang,Meng Cheng,Jingzhe Wang,Rui Wang,Xu Chen,Chunyu Zhang,Yuntong Yang,Tongjie Ji,Min Liu,Jing Zhang,Chunlong Zhong","doi":"10.1093/nar/gkaf939","DOIUrl":"https://doi.org/10.1093/nar/gkaf939","url":null,"abstract":"G-quadruplexes (G4s) are noncanonical DNA structures that promote genomic instability, particularly in α-thalassemia/mental retardation X-linked (ATRX)-deficient gliomas. Although TOP2B has been implicated in chromatin remodeling, its role in G4 resolution remains poorly understood. Here, we identify TOP2B as a previously unrecognized regulator of G4 homeostasis and show that it functionally cooperates with ATRX to facilitate G4 resolution during DNA replication. Disruption of this pathway by CX-5461, a small molecule originally developed as an RNA polymerase I inhibitor, leads to G4 accumulation, replication stress, and DNA damage. Mechanistically, CX-5461 acts as a TOP2B poison that selectively impairs TOP2B binding at G4 sites, alters replication fork dynamics, and induces MRE11-dependent degradation of stalled forks. These effects are strongly enhanced in ATRX-deficient glioma cells, where TOP2B plays a dominant role in G4 regulation. While etoposide similarly induces G4-related DNA damage, it does not affect the ATRX-TOP2B interaction, highlighting CX-5461's unique mechanism. Our findings establish TOP2B as a critical player in G4 resolution, reveal CX-5461's dual function as a TOP2B poison and G4 stabilizer, and propose G4-associated replication stress as a potential therapeutic target in ATRX-deficient gliomas.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"54 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Eps2Fold: a rapid method to characterize G-quadruplex DNA structures using single absorbance spectra. Eps2Fold：一种使用单吸光度光谱快速表征g -四重体DNA结构的方法。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf953

Eric Largy,Aurore Guédin,Amani Kabbara,Jean-Louis Mergny,Samir Amrane

{"title":"Eps2Fold: a rapid method to characterize G-quadruplex DNA structures using single absorbance spectra.","authors":"Eric Largy,Aurore Guédin,Amani Kabbara,Jean-Louis Mergny,Samir Amrane","doi":"10.1093/nar/gkaf953","DOIUrl":"https://doi.org/10.1093/nar/gkaf953","url":null,"abstract":"G-rich oligonucleotides can fold into non-canonical secondary structures called G-quadruplexes (G4s), consisting of stacked G-tetrads, i.e. planar arrays of four guanines connected by eight hydrogen bonds and coordinating cations such as K+ and Na+. G4s are remarkably polymorphic structures, which enables them to participate in various biological processes and find applications in nanotechnology. The development of simple and rapid assays to better understand how and when G4s form remains very important. Here, we present Eps2Fold (Epsilon-to-Fold), a method for detection and characterization of G4 conformations by simply measuring a single UV-absorbance spectrum. Eps2Fold is conceptually similar to isothermal differential spectra or thermal differential spectra but is generated by the subtraction of an experimentally recorded UV absorbance spectrum of the G4 in its folded state and a calculated UV absorbance spectrum that mimics the G4 in its unfolded state. Through comprehensive biophysical and principal component analysis (PCA) analysis of thirty G4-forming oligonucleotides, we demonstrate that Eps2Fold provides spectral signatures with unexpectedly high structural resolution remarkably similar to that obtained with circular dichroism spectra. Both techniques allow precise topology assignment based on the number and composition of stacked syn or anti guanines glycosidic bond angle stacks. The spectral differences between conformers are subtle and best analyzed using multivariate statistical approaches such as PCA rather than visual inspection alone. We provide an open-source GUI program to facilitate such analysis. Users simply upload the UV absorbance spectrum of the G4 on the web application (https://github.com/EricLarG4/Eps2Fold); structural analysis will run automatically. Eps2Fold represents a rapid and inexpensive structural approach enabling precise characterization of G4 structures from a single UV absorbance spectrum.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"95 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

MetaflowX: a scalable and resource-efficient workflow for multi-strategy metagenomic analysis. MetaflowX：用于多策略宏基因组分析的可扩展且资源高效的工作流。

IF 13.1 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf954

Yan Xia, Lifeng Liang, Xiaokai Wang, Zixiang Chen, Jin Liu, Ying Yang, Hailiang Xie, Zhimin Ding, Xiaoting Huang, Shibin Long, Zhifeng Wang, Xiaoqiang Xu, Chao Ding, Qiyi Chen, Qiang Feng

{"title":"MetaflowX: a scalable and resource-efficient workflow for multi-strategy metagenomic analysis.","authors":"Yan Xia, Lifeng Liang, Xiaokai Wang, Zixiang Chen, Jin Liu, Ying Yang, Hailiang Xie, Zhimin Ding, Xiaoting Huang, Shibin Long, Zhifeng Wang, Xiaoqiang Xu, Chao Ding, Qiyi Chen, Qiang Feng","doi":"10.1093/nar/gkaf954","DOIUrl":"10.1093/nar/gkaf954","url":null,"abstract":"Microbiomes play crucial roles in diverse ecosystems, spanning environmental, agricultural, and human health domains. However, in-depth metagenomic data analysis presents significant technical and resource challenges, particularly at scale. Existing computational pipelines are typically limited to either reference-based or reference-free approaches and exhibit inefficiencies in process large datasets. Here, we introduce MetaflowX (https://github.com/01life/MetaflowX), an open-resource workflow integrating both analytical paradigms for enhanced metagenomic investigations. This modular framework encompasses short-read quality control, rapid microbial profiling, hybrid contig assembly and binning, high-quality metagenome-assembled genome (MAG) identification, as well as bin refinement and reassembly. Benchmarking tests showed that MetaflowX completed full metagenomic analyses up to 14-fold faster and with 38% less disk usage than existing workflows. It also recovered the highest number of high-quality and taxonomically diverse MAGs. A dedicated reassembly module further improved MAG quality, increasing completeness by 5.6% and reducing contamination by 53% on average. Functional annotation modules enable detection of key features, including virulence and antibiotic resistance genes. Designed for extensibility, MetaflowX provides an efficient solution addressing current and emerging demands in large-scale metagenomic research.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 18","pages":""},"PeriodicalIF":13.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

GASZ directly recruits MILI to the intermitochondrial cement for piRNA biogenesis and male germ cell development. GASZ直接将MILI招募到间歇性的线粒体水泥中，以促进piRNA的生物发生和雄性生殖细胞的发育。

IF 13.1 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf957

Junru Miao, Zhaoran Zhang, Duong Nguyen, Hanben Wang, Danella Gong, Maddison Marshall, Yinjiao Xu, Huirong Xie, Chuanyun Wang, Jingjing Zhang, Yongsheng Wang, Yuan Wang

{"title":"GASZ directly recruits MILI to the intermitochondrial cement for piRNA biogenesis and male germ cell development.","authors":"Junru Miao, Zhaoran Zhang, Duong Nguyen, Hanben Wang, Danella Gong, Maddison Marshall, Yinjiao Xu, Huirong Xie, Chuanyun Wang, Jingjing Zhang, Yongsheng Wang, Yuan Wang","doi":"10.1093/nar/gkaf957","DOIUrl":"10.1093/nar/gkaf957","url":null,"abstract":"Repressing transposable elements via piRNAs represents a critical defense mechanism for germ cells to maintain genomic integrity. The primary piRNA biogenesis largely occurs at intermitochondrial cement (IMC), which is characterized by uniquely clustered mitochondria and ribonucleoproteins as \"cementing material.\" RNA-binding proteins at IMC, such as MILI, are essential for piRNA biogenesis. However, MILI proteins do not possess mitochondrial localization signals; thus, they must rely on other proteins to functionally communicate with IMC. In this study, we identified GASZ as a crucial interacting partner for MILI at IMC from prospermatogonia to spermatocytes. We found that GASZ proteins at mitochondria directly recruited MILI to IMC for piRNA biogenesis. Abolishing GASZ-MILI interaction in the embryonic germ cells reduced fetal piRNA level, increased transposon expression, and compromised spermatogonial and spermatocyte development during the first wave of spermatogenesis. In addition, disrupting GASZ-MILI interaction in adulthood significantly impaired spermatogenesis, with reduced spermatocyte and spermatid formation, proving that MILI and GASZ partner together to regulate steady-state spermatogenesis. Taken together, by revealing critical GASZ-MILI interaction at IMC and defining its impact on spermatogenesis, our findings critically inform how the piRNA biogenesis machinery is constructed via protein interactions to preserve germline DNA integrity for proper germ cell development.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 18","pages":""},"PeriodicalIF":13.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12507516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Rapid CRISPR-Cas9 target-strand nicking can provide phage resistance by reducing DNA abundance. 快速CRISPR-Cas9靶链缺口可以通过降低DNA丰度提供噬菌体抗性。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf900

Giang T Nguyen,Akshara Raju,Michael A Schelling,Dipali G Sashital

{"title":"Rapid CRISPR-Cas9 target-strand nicking can provide phage resistance by reducing DNA abundance.","authors":"Giang T Nguyen,Akshara Raju,Michael A Schelling,Dipali G Sashital","doi":"10.1093/nar/gkaf900","DOIUrl":"https://doi.org/10.1093/nar/gkaf900","url":null,"abstract":"Cas9 is an RNA-guided immune endonuclease that provides bacterial defense against bacteriophages. Cas9 relies on divalent metal ions for cleavage catalysis by two domains, HNH and RuvC, and to facilitate conformational changes that are required for cleavage activation. While Cas9 typically produces double-strand breaks (DSBs) in DNA targets, we observed that reduced, physiologically relevant Mg2+ concentrations can result in a slow rate of non-target strand cleavage by RuvC. This raised the question of whether rapid target-strand nicking by the Cas9 HNH domain is sufficient to provide protection against phage. To address this, we tested phage protection by Cas9 nickases, in which only the HNH or RuvC domain is catalytically active. We find that nicking by HNH, but not RuvC, can be sufficient to provide immunity. Target-strand nicking prevents phage DNA accumulation and can reduce the susceptibility of Cas9 to viral escape. Cleavage by RuvC is strongly impaired in the presence of other biomolecules that can compete for binding of free Mg2+, preventing formation of a DSB. Overall, our results suggest that HNH cleavage may occur more rapidly than RuvC cleavage under physiological conditions, resulting in an initial target-strand nick that may be sufficient to provide CRISPR-mediated immunity.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"11 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145116632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs. DNA聚合酶kappa是醛类ICLs的主要翻译合成聚合酶。

IF 14.9 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf875

Roxanne V van der Sluijs,Alexander E E Verkennis,Michael R Hodskinson,Jamie Barnett,Victoria M Cruz,Miguel Hernandez-Quiles,Themistoklis Liolios,Sally B Morton,Aiko Hendrikx,Collin Bos,Harm Post,Christopher L Millington,Clément Rouillon,Giulia Ricci,Francesca Mattiroli,David M Williams,Maarten Altelaar,Michiel Vermeulen,K J Patel,Puck Knipscheer

{"title":"DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.","authors":"Roxanne V van der Sluijs,Alexander E E Verkennis,Michael R Hodskinson,Jamie Barnett,Victoria M Cruz,Miguel Hernandez-Quiles,Themistoklis Liolios,Sally B Morton,Aiko Hendrikx,Collin Bos,Harm Post,Christopher L Millington,Clément Rouillon,Giulia Ricci,Francesca Mattiroli,David M Williams,Maarten Altelaar,Michiel Vermeulen,K J Patel,Puck Knipscheer","doi":"10.1093/nar/gkaf875","DOIUrl":"https://doi.org/10.1093/nar/gkaf875","url":null,"abstract":"DNA interstrand crosslinks (ICLs) are highly cytotoxic lesions that block essential cellular processes like replication and transcription. Endogenous ICLs can be induced by reactive aldehydes produced during normal cellular metabolism. Defective repair of these aldehyde-induced ICLs is associated with Fanconi anaemia (FA), a cancer predisposition syndrome. We previously showed that acetaldehyde-induced ICLs are repaired by the FA pathway and a novel excision-independent pathway. Here, we demonstrate that ICLs induced by acrolein, another cellular aldehyde, are also repaired by both pathways, establishing the generality of aldehyde ICL repair. Focusing on the FA pathway, we identify DNA polymerase kappa (Polκ) as the primary translesion synthesis (TLS) polymerase responsible for the insertion step during lesion bypass of unhooked aldehyde ICLs. This function requires Polκ's catalytic activity and PCNA interaction domains but is independent of Rev1 interaction. In contrast, Polκ has a non-catalytic role in the extension step of cisplatin ICL repair that is dependent on Rev1 interaction. Our work reveals a key role for Polκ in aldehyde ICL repair and provides mechanistic insights into how different ICL structures determine the choice of TLS polymerases during repair.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"2 1","pages":""},"PeriodicalIF":14.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145116737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

RNA/DNA-binding protein TDP43 regulates DNA mismatch repair genes with implications for genome stability. RNA/DNA结合蛋白TDP43调节DNA错配修复基因与基因组稳定性的影响。

IF 13.1 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf920

Vincent E Provasek, Albino Bacolla, Suganya Rangaswamy, Manohar Kodavati, Joy Mitra, Issa O Yusuf, Vikas H Malojirao, Velmarini Vasquez, Gavin W Britz, Guo-Min Li, Zuoshang Xu, Sankar Mitra, Ralph M Garruto, John A Tainer, Muralidhar L Hegde

{"title":"RNA/DNA-binding protein TDP43 regulates DNA mismatch repair genes with implications for genome stability.","authors":"Vincent E Provasek, Albino Bacolla, Suganya Rangaswamy, Manohar Kodavati, Joy Mitra, Issa O Yusuf, Vikas H Malojirao, Velmarini Vasquez, Gavin W Britz, Guo-Min Li, Zuoshang Xu, Sankar Mitra, Ralph M Garruto, John A Tainer, Muralidhar L Hegde","doi":"10.1093/nar/gkaf920","DOIUrl":"10.1093/nar/gkaf920","url":null,"abstract":"TDP43 is an RNA/DNA-binding protein increasingly recognized for its role in neurodegenerative conditions, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). As characterized by its aberrant nuclear export and cytoplasmic aggregation, TDP43 proteinopathy is a hallmark feature in over 95% of ALS/FTD cases, leading to detrimental cytosolic aggregates and a reduction in nuclear functionality in neurons. Building on our prior work linking TDP43 proteinopathy to the accumulation of DNA double-strand breaks (DSBs) in neurons, the present investigation uncovers a novel regulatory relationship between TDP43 and DNA mismatch repair (MMR) gene expression. Here, we show that TDP43 depletion or overexpression directly affects the expression of key MMR genes. Alterations include changes in MLH1, MSH2, MSH3, MSH6, and PMS2 levels across various primary cell lines, independent of their proliferative status. Our results specifically establish that TDP43 selectively influences the expression of MLH1 and MSH6 by influencing their alternative transcript splicing patterns and stability. We furthermore find that aberrant MMR gene expression is linked to TDP43 proteinopathy in two distinct ALS mouse models and in post-mortem brain and spinal cord tissues of ALS patients. Notably, MMR depletion resulted in the partial rescue of TDP43 proteinopathy-induced DNA damage and signaling. Moreover, bioinformatics analysis of the TCGA cancer database reveals significant associations between TDP43 expression, MMR gene expression, and mutational burden across multiple cancers. Collectively, our findings implicate TDP43 as a critical regulator of the MMR pathway and unveil its broad impact on the etiology of both neurodegenerative and neoplastic pathologies.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 18","pages":""},"PeriodicalIF":13.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Damage-induced phosphorylation of BRC-1/BRD-1 in meiosis preserves germline integrity. 损伤诱导的BRC-1/BRD-1在减数分裂中磷酸化可保持种系完整性。

IF 13.1 2区生物学

Nucleic Acids Research Pub Date : 2025-09-23 DOI: 10.1093/nar/gkaf945

Nuria Fernández-Fernández, Mariola Chacón, Lola P Camino, Tatiana Garcia-Muse

引用次数: 0