Communications Biology最新文献_第10页

Prediction of pathogenic mutations in human transmembrane proteins and their associated diseases via utilizing pre-trained Bio-LLMs. 利用预训练的Bio-LLMs预测人类跨膜蛋白及其相关疾病的致病性突变。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-15 DOI: 10.1038/s42003-025-08452-7

Lexin Cao, Lijun Quan, Qiufeng Chen, Bei Zhang, Zhijun Zhang, Liangchen Peng, Junkai Wang, Yelu Jiang, Liangpeng Nie, Geng Li, Tingfang Wu, Qiang Lyu

{"title":"Prediction of pathogenic mutations in human transmembrane proteins and their associated diseases via utilizing pre-trained Bio-LLMs.","authors":"Lexin Cao, Lijun Quan, Qiufeng Chen, Bei Zhang, Zhijun Zhang, Liangchen Peng, Junkai Wang, Yelu Jiang, Liangpeng Nie, Geng Li, Tingfang Wu, Qiang Lyu","doi":"10.1038/s42003-025-08452-7","DOIUrl":"10.1038/s42003-025-08452-7","url":null,"abstract":"Missense mutations can disrupt the structure and function of membrane proteins, potentially impairing key biological processes and leading to various human diseases. However, existing computational methods primarily focus on binary pathogenicity classification for general proteins, with limited approaches specifically designed for membrane proteins, and even fewer methods capable of fine-grained, multi-label classification for specific disease categories. To address this gap, we proposed MutDPAL, a deep learning method specifically designed to identify pathogenic mutations in membrane proteins and further classify such pathogenic mutations into potential diseases categories. MutDPAL utilizes two pre-trained biological large language models (Bio-LLMs), one for raw sequence features and the other for encoding transmembrane environment features. By employing a cross-attention-based disease-protein association learning approach in the context of membrane proteins, MutDPAL captures the intricate relationships between mutations and diseases, enabling accurate pathogenicity prediction and classification into 15 distinct disease categories. Experimental results demonstrate that MutDPAL outperforms existing methods in predicting membrane protein mutation pathogenicity and excels in multi-label disease classification tasks, achieving high predictive accuracy across all 15 disease categories. MutDPAL is the first to combine transmembrane environment with disease encoding features for fine-grained disease classification, offering valuable insights into the pathogenicity of missense mutations in membrane protein.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1050"},"PeriodicalIF":5.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12264167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642022","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

Deciphering the role of CAPZA2 in neurodevelopmental disorders: insights from mouse models. 解读CAPZA2在神经发育障碍中的作用：来自小鼠模型的见解。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-15 DOI: 10.1038/s42003-025-08385-1

Mei Guo, Liming Liu, Xiao Mao, Manyu Xiao, Xiaobin He, Xing Pan, Yuewen Chen, Wanying Yi, Qibin Li, Xianglan Piao, Hua Wang, Yang Du, Yong Cheng

{"title":"Deciphering the role of CAPZA2 in neurodevelopmental disorders: insights from mouse models.","authors":"Mei Guo, Liming Liu, Xiao Mao, Manyu Xiao, Xiaobin He, Xing Pan, Yuewen Chen, Wanying Yi, Qibin Li, Xianglan Piao, Hua Wang, Yang Du, Yong Cheng","doi":"10.1038/s42003-025-08385-1","DOIUrl":"10.1038/s42003-025-08385-1","url":null,"abstract":"Intellectual disability affects 1-3% of the global population, with many unidentified genetic causes. This study investigates the role of CAPZA2, an actin cytoskeleton regulator, in neurodevelopmental disorders using CAPZA2 heterozygous knockout (CAPZA2+/-) and heterozygous point mutant (CAPZA2c.G776T/+) mice. CAPZA2+/- and CAPZA2c.G776T/+ mice demonstrate notable decreases in CAPZA2 expression within the hippocampus and prefrontal cortex (PFC), crucial for learning and memory. Interestingly, the reduction of CAPZA2 in CAPZA2c.G776T/+ mice is less than 50%. Behavioral assays revealed that CAPZA2+/- mice exhibited motor dysfunction and anxiety-like behaviors, along with impairments in both spatial and non-spatial memory, accompanied by deficits in social interactions. These phenotypic manifestations are also mirrored in the CAPZA2c.G776T/+ mice, thus validating the genotype-phenotype correlation. Morphological analyses of these gene-edited mice indicate structural synaptic impairments, with increased dendritic spine density, altered spine morphology in the hippocampus, and decreased dendritic complexity in the PFC. Single-cell RNA-seq analysis of hippocampal tissue in CAPZA2+/- mice shows widespread transcriptional dysregulation, affecting neurodevelopment and synaptic function genes. The altered PSD95 and glutamate receptor levels support these findings. These insights highlight the gene's essential role in brain development and function, with potential implications for understanding and treating neurodevelopmental disorders.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1048"},"PeriodicalIF":5.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636386","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

Rapid detection and capture of clinical Escherichia coli strains mediated by OmpA-targeting nanobodies. ompa靶向纳米体介导的临床大肠杆菌的快速检测和捕获。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-14 DOI: 10.1038/s42003-025-08345-9

Michèle Sorgenfrei, Lea M Hürlimann, Andrea Printz, Fanny Wegner, Damien Morger, Fabian Ackle, Mélissa M Remy, Grzegorz Montowski, Hans-Anton Keserue, Aline Cuénod, Frank Imkamp, Adrian Egli, Peter M Keller, Markus A Seeger

{"title":"Rapid detection and capture of clinical Escherichia coli strains mediated by OmpA-targeting nanobodies.","authors":"Michèle Sorgenfrei, Lea M Hürlimann, Andrea Printz, Fanny Wegner, Damien Morger, Fabian Ackle, Mélissa M Remy, Grzegorz Montowski, Hans-Anton Keserue, Aline Cuénod, Frank Imkamp, Adrian Egli, Peter M Keller, Markus A Seeger","doi":"10.1038/s42003-025-08345-9","DOIUrl":"10.1038/s42003-025-08345-9","url":null,"abstract":"Escherichia coli is a major cause of blood stream and urinary tract infections. Owing to the spread of antimicrobial resistance, it is often treated with an inadequate antibiotic. With the aim to accelerate the diagnostics of this key pathogen, we used the flycode technology to generate nanobodies against the conserved and highly abundant outer membrane protein OmpA. Two nanobodies each recognizing a different isoform of OmpA were shown by flow cytometry to recognize > 91% of 85,680 E. coli OmpA sequences deposited in a large bacterial genome database. Crystal structures of these nanobodies in complex with the respective OmpA isoform revealed interactions with all four surface accessible loops of OmpA. Steric hindrance caused by dense O-antigen layers initially impeded reliable capture of clinical E. coli strains. By generating nanobody constructs with long linkers and by thinning the O-antigen layer through alterations to growth medium and buffers, we achieved to capture < 50 CFU/mL. Our work provides a framework to generate nanobodies for the specific and sensitive detection and capture of clinically relevant pathogenic bacteria.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1047"},"PeriodicalIF":5.2,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636387","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

Intricate interactions between fine-scale genetic structure, lifestyle, and dietary habits in the Japanese population. 日本人口精细遗传结构、生活方式和饮食习惯之间复杂的相互作用。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-12 DOI: 10.1038/s42003-025-08479-w

Yichi Chen, Kotoe Katayama, Sachiko Ishida, Seiya Imoto

{"title":"Intricate interactions between fine-scale genetic structure, lifestyle, and dietary habits in the Japanese population.","authors":"Yichi Chen, Kotoe Katayama, Sachiko Ishida, Seiya Imoto","doi":"10.1038/s42003-025-08479-w","DOIUrl":"10.1038/s42003-025-08479-w","url":null,"abstract":"The fine-scale genetic structure within populations, focusing on demographic histories and migration patterns, has been explored previously. However, limited attention has been paid to understanding how genetic structure influences lifestyle and dietary habits within an epidemiological framework. This study explores the fine-scale genetic structure within a homogeneous Japanese population using advanced unsupervised learning techniques-Principal Component Analysis (PCA), Uniform Manifold Approximation and Projection (UMAP), and Density-Based Spatial Clustering of Applications with Noise (DBSCAN)-coupled with direct-to-consumer genetic testing data. We investigate the associated genetic factors and examine the relationship between the genetic structure and geographic ancestry. Additionally, using cross-sectional data and multinomial logistic regression, we further elucidate the nuanced impacts of lifestyle and dietary factors across genetic clusters, emphasizing the importance of integrating genetic data with epidemiological research. This study introduces a new framework for genetic epidemiology that considers both genetic and environmental influences.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1046"},"PeriodicalIF":5.2,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616632","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

βTrCP facilitates MRN complex localization on chromatin to enhance DNA repair. βTrCP促进MRN复合物在染色质上的定位，促进DNA修复。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08462-5

Alejandro Belmonte-Fernández, Joaquín Herrero-Ruíz, Carmen Sáez, Miguel Á Japón, Mar Mora-Santos, Francisco Romero

{"title":"βTrCP facilitates MRN complex localization on chromatin to enhance DNA repair.","authors":"Alejandro Belmonte-Fernández, Joaquín Herrero-Ruíz, Carmen Sáez, Miguel Á Japón, Mar Mora-Santos, Francisco Romero","doi":"10.1038/s42003-025-08462-5","DOIUrl":"10.1038/s42003-025-08462-5","url":null,"abstract":"Genomic instability underlies various diseases, including cancer. This instability arises from defects in critical cellular processes, particularly those involved in DNA damage repair. Therefore, a detailed understanding of these repair mechanisms is essential for developing strategies to prevent or diagnose such diseases. The MRN complex, composed of MRE11, NBS1, and RAD50, is among the earliest elements involved in detecting DNA damage. Upon detecting DNA breaks, this complex triggers a cascade of signaling events that regulate both cell cycle arrest and DNA repair. These signaling pathways are tightly controlled by various post-translational modifications, notably ubiquitination. Although several ubiquitin ligases have been implicated in different stages of the DNA damage response, our knowledge remains limited. In this study, we reveal that βTrCP, a substrate-recognizing subunit of the SCF (SKP1/CUL1/F-box protein) ubiquitin ligase, interacts in vivo with the proteins of the MRN complex. These interactions occur in normally proliferating cells and are dependent on the GSK3 kinase. Moreover, we show that βTrCP enhances the recruitment of the MRN complex to chromatin through MRE11, thereby promoting the efficient DNA damage repair. Hence, alterations in βTrCP function affecting MRN dynamics could have severe consequences for the cell homeostasis.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1044"},"PeriodicalIF":5.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616634","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

Human and artificial visual systems share a computational principle for transforming binocular disparity into depth representation. 人类和人工视觉系统在将双眼视差转换为深度表示方面具有相同的计算原理。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08474-1

Bayu Gautama Wundari, Ichiro Fujita, Hiroshi Ban

{"title":"Human and artificial visual systems share a computational principle for transforming binocular disparity into depth representation.","authors":"Bayu Gautama Wundari, Ichiro Fujita, Hiroshi Ban","doi":"10.1038/s42003-025-08474-1","DOIUrl":"10.1038/s42003-025-08474-1","url":null,"abstract":"Our visual brain transforms small differences between images in the two eyes (binocular disparity) into coherent depth. Initially, neurons in the primary visual cortex (V1) compute the degrees of overlap between the left and right images to encode disparity. Such cross-correlation-like neurons respond to both binocularly matched and mismatched features. This ambiguous representation is refined along the visual pathway through a cross-matching computation involving additional nonlinear processing to filter out mismatches. How these representations are organized in the human visual cortex remains unclear. Using functional magnetic resonance imaging (fMRI), we show that areas V1-V3 exhibit stronger cross-correlation components, while V3A/B, V7, hV4, and hMT+ are inclined towards cross-matching. A deep neural network (DNN) trained for stereo vision undergoes a similar transformation across its layers, progressing through distinct phases that exploit dissimilar features to achieve coherent depth. This brain-DNN alignment demonstrates that human and artificial visual systems share a computational principle for robust 3D vision.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1042"},"PeriodicalIF":5.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616631","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

Changes in cortical beta power predict motor control flexibility, not vigor. 皮质β能量的变化预示着运动控制的灵活性，而不是活力。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08465-2

Emeline Pierrieau, Claire Dussard, Axel Plantey-Veux, Cloé Guerrini, Brian Lau, Léa Pillette, Nathalie George, Camille Jeunet-Kelway

{"title":"Changes in cortical beta power predict motor control flexibility, not vigor.","authors":"Emeline Pierrieau, Claire Dussard, Axel Plantey-Veux, Cloé Guerrini, Brian Lau, Léa Pillette, Nathalie George, Camille Jeunet-Kelway","doi":"10.1038/s42003-025-08465-2","DOIUrl":"10.1038/s42003-025-08465-2","url":null,"abstract":"The amplitude of beta-band activity (β power; 13-30 Hz) over motor cortical regions is used to assess and decode movement in clinical settings and brain-computer interfaces, as β power is often assumed to predict the strength of the brain's motor output, or \"vigor\". However, recent conflicting evidence challenges this assumption and underscores the need to clarify the relationship between β power and movement. In this study, sixty participants were trained to self-regulate β power using electroencephalography-based neurofeedback before performing different motor tasks. Results show that β power modulations can impact different motor variables, or the same variables in opposite directions, depending on task constraints. Importantly, downregulation of β power is associated with better task performance regardless of whether performance implied increasing or decreasing motor vigor. These findings demonstrate that β power should be interpreted as a measure of motor flexibility, which underlies adaptation to environmental constraints, rather than vigor.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1041"},"PeriodicalIF":5.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12246413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607678","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

Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis. 福替林缺乏诱导巨噬细胞抗动脉粥样硬化表型并保护高胆固醇血症小鼠免受动脉粥样硬化。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08425-w

Nattaporn Wanachottrakul, Decha Pinkaew, Sandipan Mukherjee, Preedakorn Chunhacha, Mari Nakashima, Asa A Brockman, Uttariya Pal, Hasseri B Halim, Yuhong Wei, Lena Tanaka, Hanna Huynh, Kota Ramana, Shiyou Chen, Rebecca A Ihrie, Ken Fujise

{"title":"Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.","authors":"Nattaporn Wanachottrakul, Decha Pinkaew, Sandipan Mukherjee, Preedakorn Chunhacha, Mari Nakashima, Asa A Brockman, Uttariya Pal, Hasseri B Halim, Yuhong Wei, Lena Tanaka, Hanna Huynh, Kota Ramana, Shiyou Chen, Rebecca A Ihrie, Ken Fujise","doi":"10.1038/s42003-025-08425-w","DOIUrl":"10.1038/s42003-025-08425-w","url":null,"abstract":"In the atherosclerotic intima, macrophages (MΦ) perpetuate chronic inflammation and cholesterol accumulation. Fortilin, a 172-amino-acid multifunctional protein, is abundant in the atherosclerotic intima and promotes atherogenesis, but its mechanism has remained unclear. Herein, we report that fortilin in MФ (fortilinMΦ) facilitates atherosclerosis by (a) enhancing MΦ survival, proliferation, and lipid uptake, leading to the accumulation of lipid-laden MФ in the intima and (b) inhibiting both the reverse transdifferentiation of MΦ into vascular smooth muscle cells (VSMCs) and the differentiation of mesenchymal stem cells (MSCs) into VSMCs. Mice lacking fortilinMΦ under genetically induced hypercholesterolemia (fortilinKO-MΦ-HC) exhibit drastically less atherosclerosis in their aortae compared to wild-type (fortilinWT-MΦ-HC) controls. Imaging mass cytometry reveals that the intima of fortilinKO-MΦ-HC mice contains fewer MФ but more VSMCs than that of fortilinWT-MФ-HC mice. Cell-based assays reveal that fortilin deficiency in MΦ augments low-density lipoprotein (LDL)-induced apoptosis, suppresses proliferation and foam cell formation, and boosts TGF-β1 production. Fortilin-deficient THP1 MΦ transdifferentiate into VSMCs, and their conditioned medium causes MSCs to differentiate toward VSMCs in a TGF-β1-dependent fashion. Together, these findings suggest that fortilinMΦ plays a complex facilitative role in atherogenesis and represents a viable molecular target for the treatment of atherosclerosis.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1040"},"PeriodicalIF":5.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12246171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607679","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

Altering the biophysical properties of ERC1/ELKS-driven condensates interferes with cell motility. 改变ERC1/ elks驱动凝聚物的生物物理性质会干扰细胞运动。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08470-5

Lucrezia Maria Ribolla, Marco Patrone, Massimo Degano, Martina Ramella, Ivan de Curtis

{"title":"Altering the biophysical properties of ERC1/ELKS-driven condensates interferes with cell motility.","authors":"Lucrezia Maria Ribolla, Marco Patrone, Massimo Degano, Martina Ramella, Ivan de Curtis","doi":"10.1038/s42003-025-08470-5","DOIUrl":"10.1038/s42003-025-08470-5","url":null,"abstract":"Cell migration is orchestrated by molecular networks supporting motility. The scaffolds ERC1/ELKS and Liprin-α1 sustain cell migration and invasion by assembling dynamic plasma membrane-associated platforms. ERC1/ELKS forms cytoplasmic condensates with liquid-like behavior. In this study we tested whether the ability of ERC1 to form condensates is relevant to its function in cell motility. We identified the shortest N-terminal region of ERC1 sufficient to drive phase separation in vitro and in cells. Fluorescence recovery after photobleaching confirmed the dynamic behavior of ERC1(1-244) condensates. Surprisingly, deletion of ERC1(1-244) including an intrinsically disordered region did not abolish the ability of ERC1DΔN to form condensates. Although the interactions of ERC1ΔN with partners were unaffected, the biophysical properties of ERC1ΔN condensates were altered, with consequences on cell motility. These findings highlight the importance of ERC1/ELKS to assemble functional networks, and show that altering the properties of ERC1-driven condensates interferes with tumor cell motility.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1045"},"PeriodicalIF":5.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616630","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

TRIM33 loss reduces androgen receptor transcriptional output and H2BK120 ubiquitination. TRIM33缺失减少雄激素受体转录输出和H2BK120泛素化。

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-07-11 DOI: 10.1038/s42003-025-08449-2

Nils Eickhoff, Janina Janetzko, Nuno Padrão, Sebastian Gregoricchio, Joseph C Siefert, Liesbeth Hoekman, Simon Linder, Onno Bleijerveld, Andries M Bergman, Wilbert Zwart

引用次数: 0