Molecular Systems Biology最新文献_第10页

Transcriptomic profiling of shed cells enables spatial mapping of cellular turnover in human organs. 脱壳细胞的转录组学分析使人类器官中细胞周转的空间定位成为可能。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-02 DOI: 10.1038/s44320-025-00154-w

Tal Barkai, Oran Yakubovsky, Yael Korem Kohanim, Keren Bahar Halpern, Sapir Shir, Noa Oren, Michal Fine, Paz Kelmer, Amit Talmon, Alon Israeli, Niv Pencovich, Ron Pery, Ido Nachmany, Shalev Itzkovitz

{"title":"Transcriptomic profiling of shed cells enables spatial mapping of cellular turnover in human organs.","authors":"Tal Barkai, Oran Yakubovsky, Yael Korem Kohanim, Keren Bahar Halpern, Sapir Shir, Noa Oren, Michal Fine, Paz Kelmer, Amit Talmon, Alon Israeli, Niv Pencovich, Ron Pery, Ido Nachmany, Shalev Itzkovitz","doi":"10.1038/s44320-025-00154-w","DOIUrl":"10.1038/s44320-025-00154-w","url":null,"abstract":"Single-cell atlases provide valuable insights into gene expression states but lack information on cellular dynamics. Understanding cell turnover rates-the time between a cell's birth and death-can shed light on stemness potential and susceptibility to damage. However, measuring turnover rates in human organs has been a significant challenge. In this study, we integrate transcriptomic data from both tissue and shed cells to assign turnover scores to individual cells, leveraging their expression profiles in spatially resolved expression atlases. By performing RNA sequencing on shed cells from the upper gastrointestinal tract, collected via nasogastric tubes, we infer turnover rates in the human esophagus, stomach, and small intestine. In addition, we analyze colonic fecal washes to map turnover patterns in the human large intestine. Our findings reveal a subset of short-lived, interferon-stimulated colonocytes within a distinct pro-inflammatory microenvironment. Our approach introduces a dynamic dimension to single-cell atlases, offering broad applicability across different organs and diseases.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1778-1792"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213197","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

PatientProfiler: building patient-specific signaling models from proteogenomic data. PatientProfiler：从蛋白质基因组学数据中构建患者特异性信号模型。

IF 7.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-10 DOI: 10.1038/s44320-025-00160-y

Veronica Lombardi, Lorenzo Di Rocco, Eleonora Meo, Veronica Venafra, Elena Di Nisio, Valerio Perticaroli, Mihail Lorentz Nicolaeasa, Chiara Cencioni, Francesco Spallotta, Rodolfo Negri, Francesca Sacco, Livia Perfetto

{"title":"PatientProfiler: building patient-specific signaling models from proteogenomic data.","authors":"Veronica Lombardi, Lorenzo Di Rocco, Eleonora Meo, Veronica Venafra, Elena Di Nisio, Valerio Perticaroli, Mihail Lorentz Nicolaeasa, Chiara Cencioni, Francesco Spallotta, Rodolfo Negri, Francesca Sacco, Livia Perfetto","doi":"10.1038/s44320-025-00160-y","DOIUrl":"10.1038/s44320-025-00160-y","url":null,"abstract":"Deciphering patient-specific mechanisms of cancer cell reprogramming remains a crucial challenge in systems oncology, as it is key to improving patient diagnosis and treatment. For this reason, comprehensive and patient-specific multi-omic characterization of tumor specimens has become increasingly common in clinical practice. Here, we developed PatientProfiler, a computational workflow that integrates proteogenomic data with curated causal interaction networks to generate mechanistic models of signal transduction for individual patients. PatientProfiler allows multi-omic data analysis and standardization, generation of patient-specific mechanistic models of signal transduction, and extraction of network-based prognostic biomarkers. We successfully benchmarked the tool on proteogenomic and clinical data derived from 122 biopsies of treatment-naïve breast cancer, available through the CPTAC portal. We identified patient-specific mechanistic models that recapitulate oncogenic signaling pathways. In-depth topological exploration of these networks revealed seven subgroups of patients, associated with unique transcriptomic signatures and distinct prognostic values. We identified well-known Basal-like 1 and 2 subtypes, while also highlighting distinct mechanistic drivers such as the MYC-CDK4/6 axis or NF-kappaB-mediated inflammatory programs. Beyond breast cancer, PatientProfiler offers a generalizable framework to transform cohort-level multi-omic data into interpretable mechanistic models, making it applicable across diverse cancer types and other complex diseases.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1845-1865"},"PeriodicalIF":7.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12672659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275238","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

High-throughput 3D engineered paediatric tumour models for precision medicine. 高精度医学的高通量3D工程儿科肿瘤模型。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-01 DOI: 10.1038/s44320-025-00152-y

MoonSun Jung, Valentina Poltavets, Joanna N Skhinas, Gabor Tax, Alvin Kamili, Jinhan Xie, Sarah Ghamrawi, Philipp Graber, Jie Mao, Marie Wong-Erasmus, Louise Cui, Kathleen Kimpton, Pooja Venkat, Chelsea Mayoh, Angela Lin, Emmy D G Fleuren, Ashleigh M Fordham, Zara Barger, John Grady, David M Thomas, Eric Y Du, Nicole S Graf, Mark J Cowley, Andrew J Gifford, Jamie I Fletcher, Loretta M S Lau, M Emmy M Dolman, J Justin Gooding, Maria Kavallaris

{"title":"High-throughput 3D engineered paediatric tumour models for precision medicine.","authors":"MoonSun Jung, Valentina Poltavets, Joanna N Skhinas, Gabor Tax, Alvin Kamili, Jinhan Xie, Sarah Ghamrawi, Philipp Graber, Jie Mao, Marie Wong-Erasmus, Louise Cui, Kathleen Kimpton, Pooja Venkat, Chelsea Mayoh, Angela Lin, Emmy D G Fleuren, Ashleigh M Fordham, Zara Barger, John Grady, David M Thomas, Eric Y Du, Nicole S Graf, Mark J Cowley, Andrew J Gifford, Jamie I Fletcher, Loretta M S Lau, M Emmy M Dolman, J Justin Gooding, Maria Kavallaris","doi":"10.1038/s44320-025-00152-y","DOIUrl":"10.1038/s44320-025-00152-y","url":null,"abstract":"Precision medicine for paediatric and adult cancers that incorporates drug sensitivity profiling can identify effective therapies for individual patients. However, obtaining adequate biopsy samples for high-throughput (HTP) screening remains challenging, with tumours needing to be expanded in culture or patient-derived xenografts, this is time-consuming and often unsuccessful. Herein, we have developed paediatric patient-derived tumour models using an engineered extracellular matrix (ECM) tissue mimic hydrogel system and HTP 3D bioprinting. Gene expression analysis from a neuroblastoma and sarcoma paediatric patient cohort identified key components of the ECM in these tumour types. Engineered hydrogels with ECM-mimic peptides were used to bioprint and create patient-specific tumouroids using patient-derived cells from xenograft models, and the approach was further confirmed on direct patient tumour samples. Bioprinted tumouroids from the PDX models recapitulated the genetic and phenotypic characteristics of the original tumours and retained tumourigenicity. HTP drug screening of these models identified individualised drug sensitivities. Our approach offers a timely and clinically relevant technology platform for precision medicine in paediatric cancers, potentially transforming preclinical testing across multiple cancer types.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1748-1777"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206934","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

A scheduler for rhythmic gene expression. 节律性基因表达的调度器。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-10 DOI: 10.1038/s44320-025-00155-9

Dimos Gaidatzis, Maike Graf-Landua, Stephen P Methot, Michaela Wölk, Giovanna Brancati, Yannick P Hauser, Milou W M Meeuse, Smita Nahar, Kathrin Braun, Marit van der Does, Sirisha Aluri, Hubertus Kohler, Sebastien Smallwood, Helge Großhans

{"title":"A scheduler for rhythmic gene expression.","authors":"Dimos Gaidatzis, Maike Graf-Landua, Stephen P Methot, Michaela Wölk, Giovanna Brancati, Yannick P Hauser, Milou W M Meeuse, Smita Nahar, Kathrin Braun, Marit van der Does, Sirisha Aluri, Hubertus Kohler, Sebastien Smallwood, Helge Großhans","doi":"10.1038/s44320-025-00155-9","DOIUrl":"10.1038/s44320-025-00155-9","url":null,"abstract":"Genetic oscillators drive precisely timed gene expression, crucial for development and physiology. Using the C. elegans molting clock as a model, we investigate how oscillators can schedule the orderly expression of thousands of genes. Single-cell RNA sequencing reveals a broad peak phase dispersion in individual tissues, mirrored by rhythmic changes in chromatin accessibility at thousands of regulatory elements identified by time-resolved ATAC-seq. We develop a linear model to predict chromatin dynamics based on the binding of >200 transcription factors. This identifies nine key regulators acting additively to determine the peak phase and amplitude of each regulatory element. Strikingly, these factors can also generate constitutive, non-rhythmic activity through destructive interference. Validating its power, the model accurately predicts the impact of GRH-1/Grainyhead perturbation on both chromatin and transcript dynamics. This work provides a conceptual framework for understanding how combinatorial, non-cooperative transcription factor binding schedules complex gene expression patterns in development and other dynamic biological processes.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1793-1821"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275209","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

Fast and furious: mapping epithelial cellular turnover into intestinal transcriptomic atlases. 速度与激情：将上皮细胞转化成肠道转录组图谱。

IF 7.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-02 DOI: 10.1038/s44320-025-00156-8

Christoph Kilian, Lorenz Adlung

引用次数: 0

Molecular Systems Biology at 20: reflecting on the past, envisioning the future. 20岁分子系统生物学：反思过去，展望未来。

IF 7.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-11-20 DOI: 10.1038/s44320-025-00170-w

Poonam Bheda, Jingyi Hou, Ruedi Aebersold, Uri Alon, Joel S Bader, Lee Bardwell, Edison T Liu, James C W Locke, Matthias Mann, Andrew J Millar, Felix Naef, Yitzhak Pilpel, Ron Shamir, Dennis Vitkup

引用次数: 0

Hominoid-specific transposable elements reshaped neural crest migration in craniofacial development. 类人猿特有的转座因子在颅面发育过程中重塑神经嵴迁移。

IF 7.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-09-22 DOI: 10.1038/s44320-025-00151-z

Laura Deelen, Zoe H Mitchell, Martina Demurtas, Andria Koulle, Beatriz Garcia Del Valle, Marco Trizzino

{"title":"Hominoid-specific transposable elements reshaped neural crest migration in craniofacial development.","authors":"Laura Deelen, Zoe H Mitchell, Martina Demurtas, Andria Koulle, Beatriz Garcia Del Valle, Marco Trizzino","doi":"10.1038/s44320-025-00151-z","DOIUrl":"10.1038/s44320-025-00151-z","url":null,"abstract":"Craniofacial development is evolutionarily conserved, yet subtle changes in its regulatory network drive species-specific traits. Transposable elements (TEs) contribute to genome evolution, but their role in cranial neural crest cells (CNCCs) remains unclear. Here, we investigate the domestication of hominoid-specific TEs (LTR5Hs and SVAs) as enhancers during human CNCC specification, a process critical for vertebrate craniofacial development. Using human iPSC-derived CNCCs, we identified ~515 hominoid-specific TEs functioning as enhancers, including ~250 human-specific, predominantly LTR5Hs. These elements are enriched for CNCC coordinator motifs, are bound by the CNCC signature factor TWIST1, and their enhancer activity appears largely CNCC-specific. CRISPR-interference targeting ~75% of these active TEs led to widespread transcriptional dysregulation of genes involved in neural crest migration, and two orthogonal functional assays confirmed that CNCC migration is impaired upon TE repression. Finally, genes near human-specific TEs showed higher expression in human CNCCs compared to chimpanzee CNCCs, but TE repression restored gene expression to chimpanzee levels. These findings highlight how young TEs were domesticated to fine-tune CNCC regulatory networks, potentially contributing to lineage-specific craniofacial evolution.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1731-1747"},"PeriodicalIF":7.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125259","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

Methylation reprogramming associated with aggressive prostate cancer and ancestral disparities. 甲基化重编程与侵袭性前列腺癌和祖先差异相关。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-07 DOI: 10.1038/s44320-025-00153-x

Jenna Craddock, Pavlo Lutsik, Pamela X Y Soh, Melanie Louw, Md Mehedi Hasan, Sean M Patrick, Shingai B A Mutambirwa, Phillip D Stricker, Hagen E A Förtsch, M S Riana Bornman, Clarissa Gerhäuser, Vanessa M Hayes

{"title":"Methylation reprogramming associated with aggressive prostate cancer and ancestral disparities.","authors":"Jenna Craddock, Pavlo Lutsik, Pamela X Y Soh, Melanie Louw, Md Mehedi Hasan, Sean M Patrick, Shingai B A Mutambirwa, Phillip D Stricker, Hagen E A Förtsch, M S Riana Bornman, Clarissa Gerhäuser, Vanessa M Hayes","doi":"10.1038/s44320-025-00153-x","DOIUrl":"10.1038/s44320-025-00153-x","url":null,"abstract":"African men are disproportionately impacted by aggressive prostate cancer (PCa). The key to this disparity is both genetic and environmental factors, alluding to epigenetic modifications. However, African-inclusive prostate tumour DNA methylation studies are lacking. Assembling a multi-geo-ancestral prostate tissue cohort, including men with (57 African, 48 European, 23 Asian) or without (65 African) PCa, we interrogate for genome-wide differential methylation. Overall, methylation appears to be driven by ancestry over geography (152 southern Africa, 41 Australia). African tumours show substantial heterogeneity, with universal hypermethylation indicating more pervasive epigenetic silencing, encompassing PCa suppressor genes and enhancer-targeted binding motifs. Conversely, African tumour-associated heterochromatic hypomethylation suggests chromatin relaxation and developmental pathway activation via enhancer targets. Notably, non-prostate lineage elements appeared preferentially exploited in African tumorigenesis, with ancestry potentially influencing the extent of lineage-inappropriate activation, and tumour progression marked by repression of developmental regulators. Together, these findings point to extensive epigenetic plasticity in African tumours, with intergenic regulatory remodelling promoting genomic instability, metastatic potential and aggressive disease phenotypes.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1676-1701"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244806","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

Machine learning-guided deconvolution of plasma protein levels. 机器学习引导的血浆蛋白水平反卷积。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-09 DOI: 10.1038/s44320-025-00158-6

Maik Pietzner, Carl Beuchel, Kamil Demircan, Julian Hoffmann Anton, Wenhuan Zeng, Werner Römisch-Margl, Summaira Yasmeen, Burulça Uluvar, Martijn Zoodsma, Mine Koprulu, Gabi Kastenmüller, Julia Carrasco-Zanini, Claudia Langenberg

{"title":"Machine learning-guided deconvolution of plasma protein levels.","authors":"Maik Pietzner, Carl Beuchel, Kamil Demircan, Julian Hoffmann Anton, Wenhuan Zeng, Werner Römisch-Margl, Summaira Yasmeen, Burulça Uluvar, Martijn Zoodsma, Mine Koprulu, Gabi Kastenmüller, Julia Carrasco-Zanini, Claudia Langenberg","doi":"10.1038/s44320-025-00158-6","DOIUrl":"10.1038/s44320-025-00158-6","url":null,"abstract":"Proteomic techniques now measure thousands of proteins circulating in blood at population scale, but successful translation into clinically useful protein biomarkers is hampered by our limited understanding of their origins. Here, we use machine learning to systematically identify a median of 20 factors (range: 1-37) out of >1800 participant and sample charateristics that jointly explained an average of 19.4% (max. 100.0%) of the variance in plasma levels of ~3000 protein targets among 43,240 individuals. Proteins segregated into distinct clusters according to their explanatory factors, with modifiable characteristics explaining more variance compared to genetic variation (median: 10.0% vs 3.9%), and factors being largely consistent across the sexes and ancestral groups. We establish a knowledge graph that integrates our findings with genetic studies and drug characteristics to guide identification of potential drug target engagement markers. We demonstrate the value of our resource by identifying disease-specific biomarkers, like matrix metalloproteinase 12 for abdominal aortic aneurysm, and by developing a widely applicable framework for phenotype enrichment (R package: https://github.com/comp-med/r-prodente ). All results are explorable via an interactive web portal ( https://omicscience.org/apps/prot_foundation ).","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1822-1844"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12672695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145258557","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

Transition between cell states of sensitivity reveals molecular vulnerability of drug-tolerant cells. 细胞敏感状态之间的转变揭示了耐药细胞的分子脆弱性。

IF 6.7 1区生物学

Molecular Systems Biology Pub Date : 2025-12-01 Epub Date: 2025-10-01 DOI: 10.1038/s44320-025-00150-0

Ludovic Peyre, Marielle Péré, Mickael Meyer, Benjamin Bian, Marina Moureau-Barbato, Walid Djema, Bernard Mari, Georges Vassaux, Jérémie Roux

{"title":"Transition between cell states of sensitivity reveals molecular vulnerability of drug-tolerant cells.","authors":"Ludovic Peyre, Marielle Péré, Mickael Meyer, Benjamin Bian, Marina Moureau-Barbato, Walid Djema, Bernard Mari, Georges Vassaux, Jérémie Roux","doi":"10.1038/s44320-025-00150-0","DOIUrl":"10.1038/s44320-025-00150-0","url":null,"abstract":"Drug-tolerant cells to pro-apoptotic treatments exhibit transient resistance to subsequent challenges, which can be sustained via transcriptional and translational regulations. Although persister cells have been described in other cell death modalities, how they respond to subsequent treatments that are different from the one they originate from remains less explored. Here we show that drug-tolerant cells to pro-apoptotic treatments exhibit a reduced capacity to activate caspase-8, as well as higher levels of RIPK3 protein expression. As this apoptosis-tolerant cell state exhibits features of vulnerability to necroptosis, we show that alternating from apoptotic to necroptotic treatments increases cell response compared to drug holiday or sustained treatment. To gain insights on these transitions between states of vulnerability to cell death, we developed a compartmental model explaining the emergence of drug-tolerant cell populations, and the fluxes between drug-sensitivity states. We found that drug-sensitivity states coexist in a clonal population of cancer cells with continuous transitions between them, which are sufficient to explain both the sustained resistance to repeated treatments and how alternating drug treatments ameliorates the overall treatment efficacy.","PeriodicalId":18906,"journal":{"name":"Molecular Systems Biology","volume":" ","pages":"1702-1730"},"PeriodicalIF":6.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12673137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206929","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