The FEBS journal最新文献_第7页

Velamins: green-light-emitting calcium-regulated photoproteins isolated from the ctenophore Velamen parallelum. Velamins：从栉水母Velamen parallelum中分离出来的发出绿色光的钙调节光蛋白。

The FEBS journal Pub Date : 2025-04-18 DOI: 10.1111/febs.70096

Douglas M M Soares, Gabriela A Galeazzo, Germán G Sgro, Gabriela V de Moraes, Leora Kronenberg, Emmanuella Borukh, Alvaro E Migotto, David F Gruber, John S Sparks, Vincent A Pieribone, Cassius V Stevani, Anderson G Oliveira

{"title":"Velamins: green-light-emitting calcium-regulated photoproteins isolated from the ctenophore Velamen parallelum.","authors":"Douglas M M Soares, Gabriela A Galeazzo, Germán G Sgro, Gabriela V de Moraes, Leora Kronenberg, Emmanuella Borukh, Alvaro E Migotto, David F Gruber, John S Sparks, Vincent A Pieribone, Cassius V Stevani, Anderson G Oliveira","doi":"10.1111/febs.70096","DOIUrl":"https://doi.org/10.1111/febs.70096","url":null,"abstract":"Ca2+-regulated photoproteins (CaPhs) consist of single-chain globular proteins to which coelenterazine, a widely distributed marine luminogenic substrate (the luciferin), binds along with molecular oxygen, producing a stable peroxide. Upon Ca2+ addition, CaPhs undergo conformational changes leading to the cyclization of the peroxide and the formation of a high-energy intermediate. Subsequently, its decomposition yields coelenteramide in an excited state and results in the emission of a flash of light. To date, most known CaPh systems emit blue light (λmax 465-495 nm), except for two bolinopsin isospecies that emit green light (λmax 500 nm). Here, we report the cloning and functional characterization of wild-type CaPhs capable of emitting green light: velamins, isolated from the bioluminescent ctenophore Velamen parallelum. Ten unique photoprotein-like sequences were recovered and grouped in three main clusters. Representative sequences were cloned, expressed, purified, and regenerated into the active His-tagged α-, β-, and γ-velamins. Upon injection of a calcium-containing buffer into the velamin, a flash of green light (λmax 500-508 nm) was observed across pH values ranging from 7 to 9. Whilst α-velamin isoforms exhibited the highest light emission activity, β- and γ-velamins were found to be more thermostable at higher temperatures. Velamins are the wild-type CaPhs with the longest-wavelength light emission yet reported, making them an excellent model for investigating spectral modulation mechanisms in photoproteins.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Left-handed conformations of glycyl residues may confer protection against protein aggregation. 甘酰基残基的左旋构象可能具有防止蛋白质聚集的保护作用。

The FEBS journal Pub Date : 2025-04-17 DOI: 10.1111/febs.70092

Purva Mishra, Rajesh Potlia, Kuljeet Singh Sandhu

{"title":"Left-handed conformations of glycyl residues may confer protection against protein aggregation.","authors":"Purva Mishra, Rajesh Potlia, Kuljeet Singh Sandhu","doi":"10.1111/febs.70092","DOIUrl":"https://doi.org/10.1111/febs.70092","url":null,"abstract":"The lack of Cβ atom allows glycyl to adopt left-handed Ramachandran conformations, typically disallowed for l-amino acids. The underlying significance remains under-appreciated. Through conformational analysis of glycyls at 1104 disease and 343 benign variant sites, we show that the left-handed glycyls are over-represented (odds ratio > 1.3) at disease variant sites and are evolutionarily conserved. Mutations involving l-disallowed glycyls destabilize native folding by altering free energies (P = 2.4 × 10-4). The l-disallowed glycyls are enriched at the aggregation gatekeepers, more profoundly so in thermophiles (P = 2.0 × 10-6), implying heightened selection to impede aggregation. Mutations of l-disallowed glycyls also reduce the protein solubility (P = 0.001). Due to mostly positive Φ dihedral-angle, Cα atom of l-disallowed glycyl flips to conform a crescent that likely disrupts β-strand alignment, discouraging the intermolecular aggregation of β-strands. Deep learning confirms the predictive value of l-disallowed glycyls in identifying pathogenic variants (accuracy = 0.81 vs. 0.69, area under the curve = 0.88 vs. 0.79). The findings underscore the evolutionary selection of l-disallowed conformations of glycyls to maintain proteostasis by modulating protein stability and aggregation, and suggest applications for disease-associated genetic prioritization and soluble protein design.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Allosteric modulation of protein kinase A in individuals affected by NLPD-PKA, a neurodegenerative disease in which the PRKAR1B L50R variant is expressed. NLPD-PKA（一种神经退行性疾病，其中PRKAR1B L50R变体表达）患者的蛋白激酶A变构调节

The FEBS journal Pub Date : 2025-04-17 DOI: 10.1111/febs.70098

Tal Benjamin-Zukerman, Valeria Pane, Rania Safadi-Safa, Meir Solomon, Varda Lev-Ram, Mohammad Aboraya, Anwar Dakwar, Daniela Bertinetti, Andrew Hoy, Merel O Mol, John van Swieten, Rodrigo Maillard, Friedrich W Herberg, Ronit Ilouz

{"title":"Allosteric modulation of protein kinase A in individuals affected by NLPD-PKA, a neurodegenerative disease in which the PRKAR1B L50R variant is expressed.","authors":"Tal Benjamin-Zukerman, Valeria Pane, Rania Safadi-Safa, Meir Solomon, Varda Lev-Ram, Mohammad Aboraya, Anwar Dakwar, Daniela Bertinetti, Andrew Hoy, Merel O Mol, John van Swieten, Rodrigo Maillard, Friedrich W Herberg, Ronit Ilouz","doi":"10.1111/febs.70098","DOIUrl":"https://doi.org/10.1111/febs.70098","url":null,"abstract":"Protein kinase A (PKA) is a crucial signaling enzyme in neurons, with its dysregulation being implicated in neurodegenerative diseases. Assembly of the PKA holoenzyme, comprising a dimer of heterodimers of regulatory (R) and catalytic (C) subunits, ensures allosteric regulation and functional specificity. Recently, we defined the RIβ-L50R variant as a causative mutation that triggers protein aggregation in a rare neurodegenerative disease, neuronal loss, and parkinsonism driven by a PKA mutation (NLPD-PKA). However, the mechanism underlying uncontrolled PKA allosteric regulation and its connection to the functional outcomes leading to clinical symptoms remains elusive. In this study, we established an in vitro model using patient-derived cells for a personalized approach and employed direct measurements of purified proteins to investigate disease mechanisms in a controlled environment. Structural analysis and circular dichroism spectroscopy revealed that cellular protein aggregation resulted from misfolded RIβ-subunits, preventing holoenzyme assembly and anchoring through A-kinase anchoring proteins (AKAPs). While maintaining high affinity to the C-subunit, the resulting RIβ-L50R:C heterodimer exhibits reduced cooperativity, requiring lower cAMP concentrations for dissociation. Consequently, there was an increased translocation of the C-subunit into the nucleus, impacting gene expression. We successfully controlled C-subunit translocation by introducing a mutation that decreased RIβ:C dissociation in response to elevated cAMP levels. This research thus sets the stage for developing therapeutic strategies that modulate PKA assembly and allostery, thus exerting control over the unique molecular signatures identified in the disease-associated transcriptome profile.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The G protein-coupled receptor GPR89A is a novel potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells. G蛋白偶联受体GPR89A是克服NSCLC Calu1细胞顺铂耐药的一个新的潜在治疗靶点。

The FEBS journal Pub Date : 2025-04-17 DOI: 10.1111/febs.70099

Hale Guler Kara, Eda Dogan, Vildan Bozok, Cagdas Aktan, Ece Cakiroglu, Zuhal Eroglu, Duygu Aygunes Jafari, Kemal Sami Korkmaz, Serif Senturk, Buket Kosova

{"title":"The G protein-coupled receptor GPR89A is a novel potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells.","authors":"Hale Guler Kara, Eda Dogan, Vildan Bozok, Cagdas Aktan, Ece Cakiroglu, Zuhal Eroglu, Duygu Aygunes Jafari, Kemal Sami Korkmaz, Serif Senturk, Buket Kosova","doi":"10.1111/febs.70099","DOIUrl":"https://doi.org/10.1111/febs.70099","url":null,"abstract":"Lung cancer is the most frequently diagnosed cancer type worldwide and is characterised by its high metastatic potential. Standard therapy for nonsmall cell lung cancer (NSCLC) cases includes chemotherapy with the platinum-based chemotherapeutic agent cisplatin. Although lung cancer cases respond well to cisplatin at the beginning of treatment, ~ 60% develop chemotherapy resistance during this process. In this study, a genome-wide CRISPR-Cas9-based genetic screening approach was employed to identify genes that cisplatin-resistant NSCLC Calu1 cells are more addicted to than sensitive cells. Cisplatin-resistant Calu1 cells were generated by the dose escalation method, and genome-wide CRISPR-Cas9-based genetic screening was performed with the Brunello CRISPR knockout library. Bioinformatics analyses of the obtained next-generation sequencing data revealed 63 potential candidate genes responsible for cisplatin resistance, including G protein-coupled receptor 89A (GPR89A), Poly(U) binding splicing factor 60 (PUF60), NBAS subunit of NRZ tethering complex (NBAS) and GrpE like 1, mitochondrial (GRPEL1). The GPR89A protein is located in the Golgi cisterna and Golgi-associated vesicle membrane, enables voltage-gated anion channel activity, and is involved in intracellular pH reduction. Functional studies carried out with GPR89A-knockout cisplatin-resistant Calu1 cells resulted in cell cycle arrest in the G2/M phase and increased polyploidy, and also prevented colony formation and cell migration. Cisplatin treatment, on the other hand, resulted in increased cell death by apoptosis upon cell cycle arrest in the S phase. In conclusion, this is the first study that identified GPR89A as a potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The unfolded protein response is a potential therapeutic target in pathogenic fungi. 未折叠蛋白反应是病原真菌的潜在治疗靶点。

The FEBS journal Pub Date : 2025-04-14 DOI: 10.1111/febs.70100

Hao Zhou, Jinping Zhang, Rong Wang, Ju Huang, Caiyan Xin, Zhangyong Song

{"title":"The unfolded protein response is a potential therapeutic target in pathogenic fungi.","authors":"Hao Zhou, Jinping Zhang, Rong Wang, Ju Huang, Caiyan Xin, Zhangyong Song","doi":"10.1111/febs.70100","DOIUrl":"https://doi.org/10.1111/febs.70100","url":null,"abstract":"Pathogenic fungal infections cause significant morbidity and mortality, particularly in immunocompromised patients. The frequent emergence of multidrug-resistant strains challenges existing antifungal therapies, driving the need to investigate novel antifungal agents that target new molecular moieties. Pathogenic fungi are subjected to various environmental stressors, including pH, temperature, and pharmacological agents, both in natural habitats and the host body. These stressors elevate the risk of misfolded or unfolded protein production within the endoplasmic reticulum (ER) which, if not promptly mitigated, can lead to the accumulation of these proteins in the ER lumen. This accumulation triggers an ER stress response, potentially jeopardizing fungal survival. The unfolded protein response (UPR) is a critical cellular defense mechanism activated by ER stress to restore the homeostasis of protein folding. In recent years, the regulatory role of the UPR in pathogenic fungi has garnered significant attention, particularly for its involvement in fungal adaptation, regulation of virulence, and drug resistance. In this review, we comparatively analyze the UPRs of fungi and mammals and examine the potential utility of the UPR as a molecular antifungal target in pathogenic fungi. By clarifying the specificity and regulatory functions of the UPR in pathogenic fungi, we highlight new avenues for identifying potential therapeutic targets for antifungal treatments.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Countering the effector functions of ESAT-6 protein in Mycobacterium tuberculosis: strategies for developing antimycobacterial therapeutics. 对抗ESAT-6蛋白在结核分枝杆菌中的效应功能：开发抗结核治疗的策略。

The FEBS journal Pub Date : 2025-04-11 DOI: 10.1111/febs.70084

Akshay Girish Manikoth, Manoj Kumar Bisht, Sudip Ghosh, Sangita Mukhopadhyay

引用次数: 0

Extracellular vesicles in multiple myeloma: pathogenesis and therapeutic application. 多发性骨髓瘤的细胞外囊泡：发病机制和治疗应用。

The FEBS journal Pub Date : 2025-04-09 DOI: 10.1111/febs.70093

Chloe Wylie, Rebecca Rowan, Dessi Malinova, Lisa Crawford

引用次数: 0

Unraveling the functional dynamics of Caenorhabditis elegans stress-responsive omega class GST-44. 揭示秀丽隐杆线虫应激反应omega类GST-44的功能动力学。

The FEBS journal Pub Date : 2025-04-05 DOI: 10.1111/febs.70088

Charlotte Sophia Kaiser, Milena Lubisch, Emma Schröder, Luka Ressmann, Marie Nicolaus, Dustin Leusder, Sven Moyzio, Robert Peuss, Antonio Miranda-Vizuete, Eva Liebau

{"title":"Unraveling the functional dynamics of Caenorhabditis elegans stress-responsive omega class GST-44.","authors":"Charlotte Sophia Kaiser, Milena Lubisch, Emma Schröder, Luka Ressmann, Marie Nicolaus, Dustin Leusder, Sven Moyzio, Robert Peuss, Antonio Miranda-Vizuete, Eva Liebau","doi":"10.1111/febs.70088","DOIUrl":"https://doi.org/10.1111/febs.70088","url":null,"abstract":"Glutathione transferases from the omega class are notable for their roles in redox regulation and cellular stress response. In this study, we conducted a comprehensive functional characterization of GST-44, an omega-class glutathione S-transferase (GSTO), in Caenorhabditis elegans, focusing on its role in cellular defense mechanisms against stress. Biochemical analysis revealed GSTO-specific enzymatic activities of recombinant GST-44, including dehydroascorbate reductase, thioltransferase, and arsenate reductase activities. Using transgenic GFP reporter strains, we identified predominant expression of GST-44 in the intestine and excretory H-cell, with significant upregulation observed under diverse stress conditions. Induction of GST-44 was particularly pronounced in the intestine in response to pathogen-, oxidative-, and endoplasmic reticulum stress. Notably, under arsenic stress, the expression of gst-44 was significantly upregulated in the excretory system of the worm, underscoring its critical role in mediating arsenic detoxification. Moreover, we demonstrated the induction of GST-44 using dimethyl fumarate, a highly specific mammalian Nrf-2 activator. The upregulation of GST-44 during arsenic stress was dependent not only on the oxidative stress response transcription factor SKN-1/Nrf2 but also on PHA-4. The deletion mutant strain gst-44(tm6133) exhibited reduced stress resistance and a shortened lifespan, with a highly diminished survival rate under arsenic stress compared to other CRISPR-generated C. elegans GSTO deletion mutants. Our findings highlight the essential role of GST-44 in mediating arsenic detoxification, as well as in stress adaptation and defense mechanisms in C. elegans.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Y12C mutation disrupts IMPDH cytoophidia and alters cancer metabolism. Y12C突变破坏了IMPDH嗜细胞性并改变了癌症代谢。

The FEBS journal Pub Date : 2025-04-05 DOI: 10.1111/febs.70086

Chia-Chun Chang, Min Peng, Gerson Dierley Keppeke, Li-Kuang Tsai, Ziheng Zhang, Li-Mei Pai, Li-Ying Sung, Ji-Long Liu

{"title":"Y12C mutation disrupts IMPDH cytoophidia and alters cancer metabolism.","authors":"Chia-Chun Chang, Min Peng, Gerson Dierley Keppeke, Li-Kuang Tsai, Ziheng Zhang, Li-Mei Pai, Li-Ying Sung, Ji-Long Liu","doi":"10.1111/febs.70086","DOIUrl":"https://doi.org/10.1111/febs.70086","url":null,"abstract":"Guanosine triphosphate (GTP) is a building block for DNA and RNA, and plays a pivotal role in various cellular functions, serving as an energy source, enzyme cofactor and a key component of signal transduction. The activity of the rate-limiting enzyme in de novo GTP synthesis, inosine monophosphate dehydrogenase (IMPDH), is regulated by nucleotide binding. Recent studies have illuminated that IMPDH octamers can assemble into linear polymers, adding another dimension to its enzymatic regulation. This polymerisation reduces IMPDH's sensitivity to the inhibitory effects of GTP binding, thereby augmenting its activity under conditions with elevated GTP levels. Within cells, IMPDH polymers may cluster to form the distinctive structure known as the cytoophidium, which is postulated to reflect the cellular demand for increased GTP concentrations. Nevertheless, the functional significance of IMPDH polymerisation in in vivo metabolic regulation remains unclear. In this study, we report the widespread presence of IMPDH cytoophidia in various human cancer tissues. Utilising the ABEmax base editor, we introduced a Y12C point mutation into IMPDH2 across multiple cancer cell lines. This mutation disrupts the polymerisation interface of IMPDH and prevents cytoophidium assembly. In some cancer xenografts, the absence of IMPDH polymers led to a downregulation of IMPDH, as well as the glycolytic and pentose phosphate pathways. Furthermore, mutant HeLa-cell-derived xenografts were notably smaller than their wild-type counterparts. Our data suggest that IMPDH polymerisation and cytoophidium assembly could be instrumental in modulating metabolic homeostasis in certain cancers, offering insights into the clinical relevance of IMPDH cytoophidium.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Analysis of mutually exclusive expression in cancer cells identifies a previously unknown intergenic regulatory paradigm. 对癌细胞中互斥表达的分析确定了一种以前未知的基因间调控范式。

The FEBS journal Pub Date : 2025-04-04 DOI: 10.1111/febs.70089

Ling Tang, Yuzhe Hu, Chao Wang, Wenling Han, Pingzhang Wang

{"title":"Analysis of mutually exclusive expression in cancer cells identifies a previously unknown intergenic regulatory paradigm.","authors":"Ling Tang, Yuzhe Hu, Chao Wang, Wenling Han, Pingzhang Wang","doi":"10.1111/febs.70089","DOIUrl":"https://doi.org/10.1111/febs.70089","url":null,"abstract":"Mutual exclusion of gene expression has received limited attention. Gene (expression) plasticity analysis provides an efficient way to identify highly plastic genes (HPGs) based on changes in expression rank. In this study, we quantitatively measured the expression plasticity of 19 961 protein-coding genes in 24 human cancer cell lines and identified HPGs in these cells. By comparing methods, we showed that virtual sorting and cosine similarity, rather than Pearson and Spearman rank correlations, are suitable for mutual exclusion. Mutually exclusive gene pairs were identified in each cell type. Experimental validation showed that thiol methyltransferase 1B (TMT1B; also known as METTL7B) and CD274 molecule (CD274; also known as PD-L1) were mutually exclusively expressed at either the mRNA or protein level. METTL7B negatively regulated PD-L1 expression in several cell types, and the JAK/STAT3 pathway was involved. Knockdown of METTL7B in Huh7 cells inhibited interleukin 2 (IL-2) secretion by Jurkat cells in co-culture experiments, and the inhibition was blocked by anti-PD-L1 antibodies. Therefore, this study provides an efficient method of expressional mutual exclusion and implies a newly identified intergenic regulatory paradigm.","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0