Nucleic Acids Research最新文献_第5页

Oxidative damage within alternative DNA structures results in aberrant mutagenic processing.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf066

Maha Zewail-Foote, Imee M A Del Mundo, Alex W Klattenhoff, Karen M Vasquez

{"title":"Oxidative damage within alternative DNA structures results in aberrant mutagenic processing.","authors":"Maha Zewail-Foote, Imee M A Del Mundo, Alex W Klattenhoff, Karen M Vasquez","doi":"10.1093/nar/gkaf066","DOIUrl":"10.1093/nar/gkaf066","url":null,"abstract":"Genetic instability is a hallmark of cancer, and mutation hotspots in human cancer genomes co-localize with alternative DNA structure-forming sequences (e.g. H-DNA), implicating them in cancer etiology. H-DNA has been shown to stimulate genetic instability in mammals. Here, we demonstrate a new paradigm of genetic instability, where a cancer-associated H-DNA-forming sequence accumulates more oxidative lesions than B-DNA under conditions of oxidative stress (OS), often found in tumor microenvironments. We show that OS results in destabilization of the H-DNA structure and attenuates the fold increase in H-DNA-induced mutations over control B-DNA in mammalian cells. Furthermore, the mutation spectra revealed that the damaged H-DNA-containing region was processed differently compared to H-DNA in the absence of oxidative damage in mammalian cells. The oxidatively modified H-DNA elicits differential recruitment of DNA repair proteins from both the base excision repair and nucleotide excision repair mechanisms. Altogether, these results suggest a new model of genetic instability whereby H-DNA-forming regions are hotspots for DNA damage in oxidative microenvironments, resulting in its altered mutagenic processing. Our findings provide valuable insights into the role of OS in DNA structure-induced genetic instability and may establish H-DNA-forming sequences as promising genomic biomarkers and potential therapeutic targets for genetic diseases.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11826088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414880","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

Cancer cell target discovery: comparing laboratory evolution of expanded DNA six-nucleotide alphabets with standard four-nucleotide alphabets.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf072

Sharpkate Shaker, Jun Li, Shuo Wan, Hong Xuan, Jinchen Long, Haiyan Cao, Tongxuan Wei, Qinguo Liu, Da Xu, Steven A Benner, Liqin Zhang

{"title":"Cancer cell target discovery: comparing laboratory evolution of expanded DNA six-nucleotide alphabets with standard four-nucleotide alphabets.","authors":"Sharpkate Shaker, Jun Li, Shuo Wan, Hong Xuan, Jinchen Long, Haiyan Cao, Tongxuan Wei, Qinguo Liu, Da Xu, Steven A Benner, Liqin Zhang","doi":"10.1093/nar/gkaf072","DOIUrl":"https://doi.org/10.1093/nar/gkaf072","url":null,"abstract":"Anthropogenic evolvable genetic information systems (AEGIS) are DNA-like molecules that can be copied, support laboratory in vitro evolution (LIVE), and evolve to give AegisBodies, analogs of antibodies. However, unlike DNA aptamers built from four different nucleotides, AegisBodies are currently built from six different nucleotides. Thus, six-letter AEGIS-LIVE delivers AegisBodies with greater stability in biological mixtures, more folds, and enhanced binding and catalytic power. Unlike DNA however, AEGIS has not benefited from 4 billion years of biological evolution to create AEGIS-specialized enzymes, but only a decade or so of human design. To learn whether AEGIS can nevertheless perform as well as natural DNA as a platform to create functional molecules, we compared two six-letter AegisBodies (LZH5b and LZH8) with a single standard four-letter aptamer, both evolved to bind specific cancer cells with ∼10 cycles of LIVE. Both evolved ∼50 nM affinities. Both discovered proteins on their cancer cell surfaces thought to function only inside of cells. Both can be internalized. Internalizing of LZH5b attached to an AEGIS nanotrain brings attached drugs into the cell. These data show that AEGIS-LIVE can do what four-letter LIVE can do at its limits of performance after 4 billion years of evolution of DNA-specialized enzymes, and better by a few metrics. As synthetic biologists continue to improve enzymology and analytical chemistry to support AEGIS-LIVE, this technology shoud prove increasingly useful as a tool, especially in cancer research.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458929","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

Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf084

Flavien Raynal, Kaustav Sengupta, Dariusz Plewczynski, Benoît Aliaga, Vera Pancaldi

{"title":"Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.","authors":"Flavien Raynal, Kaustav Sengupta, Dariusz Plewczynski, Benoît Aliaga, Vera Pancaldi","doi":"10.1093/nar/gkaf084","DOIUrl":"https://doi.org/10.1093/nar/gkaf084","url":null,"abstract":"Cancer cells are highly plastic, favoring adaptation to changing conditions. Genes related to basic cellular processes evolved in ancient species, while more specialized genes appeared later with multicellularity (metazoan genes) or even after mammals evolved. Transcriptomic analyses have shown that ancient genes are up-regulated in cancer, while metazoan-origin genes are inactivated. Despite the importance of these observations, the underlying mechanisms remain unexplored. Here, we study local and global epigenomic mechanisms that may regulate genes from specific evolutionary periods. Using evolutionary gene age data, we characterize the epigenomic landscape, gene expression regulation, and chromatin organization in several cell types: human embryonic stem cells, normal primary B-cells, primary chronic lymphocytic leukemia malignant B-cells, and primary colorectal cancer samples. We identify topological changes in chromatin organization during differentiation observing patterns in Polycomb repression and RNA polymerase II pausing, which are reversed during oncogenesis. Beyond the non-random organization of genes and chromatin features in the 3D epigenome, we suggest that these patterns lead to preferential interactions among ancient, intermediate, and recent genes, mediated by RNA polymerase II, Polycomb, and the lamina, respectively. Our findings shed light on gene regulation according to evolutionary age and suggest this organization changes across differentiation and oncogenesis.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458973","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

The ribosome as a platform to coordinate mRNA decay.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf049

Martin B D Müller, Thomas Becker, Timo Denk, Satoshi Hashimoto, Toshifumi Inada, Roland Beckmann

{"title":"The ribosome as a platform to coordinate mRNA decay.","authors":"Martin B D Müller, Thomas Becker, Timo Denk, Satoshi Hashimoto, Toshifumi Inada, Roland Beckmann","doi":"10.1093/nar/gkaf049","DOIUrl":"https://doi.org/10.1093/nar/gkaf049","url":null,"abstract":"Messenger RNA (mRNA) homeostasis is a critical aspect of cellular function, involving the dynamic interplay between transcription and decay processes. Recent advances have revealed that the ribosome plays a central role in coordinating mRNA decay, challenging the traditional view that free mRNA is the primary substrate for degradation. This review examines the mechanisms whereby ribosomes facilitate both the licensing and execution of mRNA decay. This involves factors such as the Ccr4-Not complex, small MutS-related domain endonucleases, and various quality control pathways. We discuss how translational fidelity, as well as the presence of nonoptimal codons and ribosome collisions, can trigger decay pathways such as nonstop decay and no-go decay. Furthermore, we highlight the direct association of canonical exonucleases, such as Xrn1 and the Ski-exosome system, with the ribosome, underscoring the ribosome's multifaceted role as a platform for regulatory processes governing mRNA stability. By integrating recent findings, this review offers a comprehensive overview of the structural basis of how ribosomes not only facilitate translation but also serve as critical hubs for mRNA decay coordination.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459132","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

Correction to 'Recruitment of homodimeric proneural factors by conserved CAT-CAT E-boxes drives major epigenetic reconfiguration in cortical neurogenesis'.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf129

引用次数: 0

An AT-hook transcription factor promotes transcription of histone, spliced-leader, and piRNA clusters.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf079

Yi-Hui Wang, Hannah L Hertz, Benjamin Pastore, Wen Tang

{"title":"An AT-hook transcription factor promotes transcription of histone, spliced-leader, and piRNA clusters.","authors":"Yi-Hui Wang, Hannah L Hertz, Benjamin Pastore, Wen Tang","doi":"10.1093/nar/gkaf079","DOIUrl":"10.1093/nar/gkaf079","url":null,"abstract":"In all three domains of life, genes with related functions can be organized into specific genomic regions known as gene clusters. In eukaryotes, histone, piRNA (Piwi-interacting RNA), and rDNA (ribosomal DNA) clusters are among the most notable clusters which play fundamental roles in chromatin formation, genome integrity, and translation, respectively. These clusters have long been thought to be regulated by distinct transcriptional mechanisms. In this study, using Caenorhabditis elegans as a model system we identify ATTF-6, a member of the AT-hook family, as a key factor for the expression of histone, piRNA, and 5S rDNA-SL1 (spliced leader 1) clusters. ATTF-6 is essential for C. elegans viability. It forms distinct nuclear foci at both piRNA and 5S rDNA-SL1 clusters. Loss of ATTF-6 leads to a depletion of histone mRNAs, SL1 transcripts, and piRNAs. Additionally, we demonstrate that ATTF-6 is required for the recruitment of USTC (Upstream Sequence Transcription Complex) to piRNA clusters, which is necessary for piRNA production. Collectively, our findings reveal a unifying role for an AT-hook transcription factor in promoting the expression of fundamental gene clusters.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11822377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409455","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

Precise gene expression deconvolution in spatial transcriptomics with STged.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf087

Jia-Juan Tu, Hong Yan, Xiao-Fei Zhang, Zhixiang Lin

{"title":"Precise gene expression deconvolution in spatial transcriptomics with STged.","authors":"Jia-Juan Tu, Hong Yan, Xiao-Fei Zhang, Zhixiang Lin","doi":"10.1093/nar/gkaf087","DOIUrl":"10.1093/nar/gkaf087","url":null,"abstract":"Spatially resolved transcriptomics (SRT) has transformed tissue biology by linking gene expression profiles with spatial information. However, sequencing-based SRT methods aggregate signals from multiple cell types within capture locations (\"spots\"), masking cell-type-specific gene expression patterns. Traditional cell-type deconvolution methods estimate cell compositions within spots but fail to resolve cell-type-specific gene expression, limiting their ability to uncover critical biological processes such as cellular interactions and microenvironmental dynamics. Here, we present STged (spatial transcriptomic gene expression deconvolution), a novel computational framework that goes beyond traditional deconvolution by reconstructing cell-type-specific gene expression profiles from mixed spots. STged integrates graph-based spatial correlations and reference-derived gene signatures using a non-negative least-squares regression framework, achieving precise and biologically meaningful deconvolution. Comprehensive simulations show that STged consistently outperforms existing methods in accuracy and robustness. Applications to human pancreatic ductal adenocarcinoma and human squamous cell carcinoma datasets reveal its capacity to identify microenvironment-specific highly variable genes, reconstruct spatial cell-cell communication networks, and resolve tissue architecture at near-single-cell resolution. In mouse kidney tissues, STged uncovers dynamic spatial gene expression patterns and distinct gene programs, advancing our understanding of tissue heterogeneity and cellular dynamics.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11838043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459017","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

XRCC1 mediates PARP1- and PAR-dependent recruitment of PARP2 to DNA damage sites.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf086

Xiaohui Lin, Kay Sze Karina Leung, Kaitlynn F Wolfe, Nicolas Call, Seema Khattri Bhandari, Xiaoyu Huang, Brian J Lee, Alan E Tomkinson, Shan Zha

{"title":"XRCC1 mediates PARP1- and PAR-dependent recruitment of PARP2 to DNA damage sites.","authors":"Xiaohui Lin, Kay Sze Karina Leung, Kaitlynn F Wolfe, Nicolas Call, Seema Khattri Bhandari, Xiaoyu Huang, Brian J Lee, Alan E Tomkinson, Shan Zha","doi":"10.1093/nar/gkaf086","DOIUrl":"10.1093/nar/gkaf086","url":null,"abstract":"Poly-ADP-ribose polymerases 1 and 2 (PARP1 and 2) are critical sensors of DNA-strand breaks and targets for cancer therapy. Upon DNA damage, PARP1 and 2 synthesize poly-ADP-ribose (PAR) chains on themselves and other substrates, facilitating DNA single-strand break repair by recruiting PAR-binding DNA repair factors, including X-ray repair cross-complementing group 1 (XRCC1) and aprataxin and polynucleotide kinase phosphatase-like factor (APLF). While diverse DNA lesions activate PARP1, PARP2 is selectively activated by 5' phosphorylated nicks. They function independently and compensate for each other. Previous studies suggest that PARP1 and its PAR chains act upstream to recruit PARP2 to DNA damage sites. Here, we report that the scaffold protein XRCC1 mediates PARP1- and PAR-dependent recruitment of PARP2 to damage sites. XRCC1-deficiency causes hyperactivation of PARP1 while attenuating micro-irradiation-induced PARP2 foci. Mechanistically, the BRCT1 domain of XRCC1 binds to PAR, while its BRCT2 domain interacts with the PARP2 catalytic domain independently of the PARP2 enzymatic activity and the LIG3 BRCT domain via residues D575 and Y576. This mode of PARP2 enrichment is important for the recruitment of certain PAR-binding proteins, such as APLF, but dispensable for others, such as the XRCC1-BRCT1 domain. These findings highlight the distinct role of PARP1 and PARP2 in PAR synthesis and uncover unexpected hierarchical roles of PARP1 and XRCC1 upstream of PARP2.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11838041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143459135","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

A systematic survey of TF function in E. coli suggests RNAP stabilization is a prevalent strategy for both repressors and activators.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf058

Sunil Guharajan, Vinuselvi Parisutham, Robert C Brewster

{"title":"A systematic survey of TF function in E. coli suggests RNAP stabilization is a prevalent strategy for both repressors and activators.","authors":"Sunil Guharajan, Vinuselvi Parisutham, Robert C Brewster","doi":"10.1093/nar/gkaf058","DOIUrl":"10.1093/nar/gkaf058","url":null,"abstract":"Transcription factors (TFs) are often classified as activators or repressors, yet these context-dependent labels are inadequate to predict quantitative profiles that emerge across different promoters. A mechanistic understanding of how different regulatory sequences shape TF function is challenging due to the lack of systematic genetic control in endogenous genes. To address this, we use a library of Escherichia coli strains with precise control of TF copy number, measuring the quantitative regulatory input-output function of 90 TFs on synthetic promoters that isolate the contributions of TF binding sequence, location, and basal promoter strength to gene expression. We interpret the measured regulation of these TFs using a thermodynamic model of gene expression and uncover stabilization of RNA polymerase as a pervasive regulatory mechanism, common to both activating and repressing TFs. This property suggests ways to tune the dynamic range of gene expression through the interplay of stabilizing TF function and RNA polymerase basal occupancy, a phenomenon we confirm by measuring fold change for stabilizing TFs across synthetic promoter sequences spanning over 100-fold basal expression. Our work deconstructs TF function at a mechanistic level, providing foundational principles on how gene expression is realized across different promoter contexts, with implications for decoding the relationship between sequence and gene expression.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374495","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

Allovalent scavenging of activation domains in the transcription factor ANAC013 gears transcriptional regulation.

IF 16.6 2区生物学

Nucleic Acids Research Pub Date : 2025-02-08 DOI: 10.1093/nar/gkaf065

Elise Delaforge, Amanda D Due, Frederik Friis Theisen, Nicolas Morffy, Charlotte O'Shea, Martin Blackledge, Lucia C Strader, Karen Skriver, Birthe B Kragelund

{"title":"Allovalent scavenging of activation domains in the transcription factor ANAC013 gears transcriptional regulation.","authors":"Elise Delaforge, Amanda D Due, Frederik Friis Theisen, Nicolas Morffy, Charlotte O'Shea, Martin Blackledge, Lucia C Strader, Karen Skriver, Birthe B Kragelund","doi":"10.1093/nar/gkaf065","DOIUrl":"10.1093/nar/gkaf065","url":null,"abstract":"Transcriptional regulation involves interactions between transcription factors, coregulators, and DNA. Intrinsic disorder is a major player in this regulation, but mechanisms driven by disorder remain elusive. Here, we address molecular communication within the stress-regulating Arabidopsis thaliana transcription factor ANAC013. Through high-throughput screening of ANAC013 for transcriptional activation activity, we identify three activation domains within its C-terminal intrinsically disordered region. Two of these overlap with acidic islands and form dynamic interactions with the DNA-binding domain and are released, not only upon binding of target promoter DNA, but also by nonspecific DNA. We show that independently of DNA binding, the RST (RCD--SRO--TAF4) domain of the negative regulator RCD1 (Radical-induced Cell Death1) scavenges the two acidic activation domains positioned vis-à-vis through allovalent binding, leading to dynamic occupation at enhanced affinity. We propose an allovalency model for transcriptional regulation, where sequentially close activation domains in both DNA-bound and DNA-free states allow for efficient regulation. The model is likely relevant for many transcription factor systems, explaining the functional advantage of carrying sequentially close activation domains.","PeriodicalId":19471,"journal":{"name":"Nucleic Acids Research","volume":"53 4","pages":""},"PeriodicalIF":16.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11811731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399058","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