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FBXO46 negatively regulates p53 activity by stabilizing Mdm2 FBXO46 通过稳定 Mdm2 负向调节 p53 的活性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-15 DOI: 10.1002/1873-3468.15055
Lai Wei, Ning Yu, Bo Yao, Yide Mei, Kailiang Zhao
{"title":"FBXO46 negatively regulates p53 activity by stabilizing Mdm2","authors":"Lai Wei,&nbsp;Ning Yu,&nbsp;Bo Yao,&nbsp;Yide Mei,&nbsp;Kailiang Zhao","doi":"10.1002/1873-3468.15055","DOIUrl":"10.1002/1873-3468.15055","url":null,"abstract":"<p>The tumor suppressor p53 plays a central role in suppressing tumor formation. Mouse double minute 2 homolog (Mdm2) serves as the principal ubiquitin E3 ligase responsible for the ubiquitination and subsequent degradation of p53. However, the regulatory mechanisms governing the Mdm2–p53 pathway are not comprehensively understood. Here, we report that F-box only protein 46 (FBXO46) directly binds to Mdm2 and inhibits its self-ubiquitination and degradation, leading to Mdm2 stabilization and subsequent Mdm2-mediated ubiquitination and degradation of p53. Functionally, FBXO46 promotes cell proliferation, accelerates G1/S cell cycle progression, and increases anchorage-independent cell growth by inhibiting p53. Collectively, these findings reveal a critical role for FBXO46 in controlling Mdm2 stability and establish FBXO46 as an important regulator of the Mdm2–p53 pathway.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 5","pages":"700-712"},"PeriodicalIF":3.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 E3 ligase HUWE1 interacts with ubiquitin non-covalently via key residues in the HECT domain E3 连接酶 HUWE1 通过 HECT 结构域中的关键残基与泛素进行非共价相互作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-14 DOI: 10.1002/1873-3468.15050
Li Sun, Haoran Zhang, Yan Li
{"title":"The E3 ligase HUWE1 interacts with ubiquitin non-covalently via key residues in the HECT domain","authors":"Li Sun,&nbsp;Haoran Zhang,&nbsp;Yan Li","doi":"10.1002/1873-3468.15050","DOIUrl":"10.1002/1873-3468.15050","url":null,"abstract":"<p>HUWE1, a HECT E3 ligase, is critical for processes like protein degradation and tumor development. Contrary to previous findings which suggested minimal non-covalent interactions between the HUWE1 HECT domain and ubiquitin, we identified a non-covalent interaction between the HUWE1 HECT N-lobe and ubiquitin using NMR spectroscopy, revealing a conserved ubiquitin-binding mode shared across HECT E3 ligases. Molecular dynamics simulations not only confirmed the stability of this interaction but also uncovered conformational changes in key residues, which likely influence binding affinity. Additionally, we highlighted the roles of both conserved and unique residues in ubiquitin binding. These findings advance our understanding of the interactions between the HUWE1 HECT domain and ubiquitin, and highlight potential targets for therapeutic intervention in the ubiquitin-proteasome pathway.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"559-570"},"PeriodicalIF":3.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Crystal structure of β-d-galactofuranosidase from Streptomyces sp. JHA19 in complex with an inhibitor provides insights into substrate specificity 来自链霉菌 JHA19 的β-d-半乳糖呋喃糖苷酶与抑制剂复合物的晶体结构揭示了底物的特异性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-14 DOI: 10.1002/1873-3468.15056
Noriki Fujio, Chihaya Yamada, Toma Kashima, Emiko Matsunaga, Robert J. Nash, Kaoru Takegawa, Shinya Fushinobu
{"title":"Crystal structure of β-d-galactofuranosidase from Streptomyces sp. JHA19 in complex with an inhibitor provides insights into substrate specificity","authors":"Noriki Fujio,&nbsp;Chihaya Yamada,&nbsp;Toma Kashima,&nbsp;Emiko Matsunaga,&nbsp;Robert J. Nash,&nbsp;Kaoru Takegawa,&nbsp;Shinya Fushinobu","doi":"10.1002/1873-3468.15056","DOIUrl":"10.1002/1873-3468.15056","url":null,"abstract":"<p><span>d</span>-Galactofuranose (Gal<i>f</i>) is widely distributed in glycoconjugates of pathogenic microbes. β-<span>d</span>-Galactofuranosidase (Gal<i>f</i>-ase) from <i>Streptomyces</i> sp. JHA19 (ORF1110) belongs to glycoside hydrolase (GH) family 2 and is the first identified Gal<i>f</i>-specific degradation enzyme. Here, the crystal structure of ORF1110 in complex with a mechanism-based potent inhibitor, <span>d</span>-iminogalactitol (<i>K</i><sub>i</sub> = 65 μ<span>m</span>) was solved. ORF1110 binds to the C5–C6 hydroxy groups of <span>d</span>-iminogalactitol with an extensive and integral hydrogen bond network, a key interaction that discriminates the substrates. The active site structure of ORF1110 is largely different from those of β-glucuronidases and β-galactosidases in the same GH2 family. A C-terminal domain of ORF1110 is predicted to be a carbohydrate-binding module family 42 that may bind Gal<i>f</i>. The structural insights into Gal<i>f</i>-ase will contribute to the investigation of therapeutic tools against pathogens.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 23","pages":"2866-2875"},"PeriodicalIF":3.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11627007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 detection of RNA modifications at single base resolution 以单碱基分辨率高通量检测 RNA 修饰。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-14 DOI: 10.1002/1873-3468.15052
Keren Ron, Joshua Kahn, Nofar Malka-Tunitsky, Aldema Sas-Chen
{"title":"High-throughput detection of RNA modifications at single base resolution","authors":"Keren Ron,&nbsp;Joshua Kahn,&nbsp;Nofar Malka-Tunitsky,&nbsp;Aldema Sas-Chen","doi":"10.1002/1873-3468.15052","DOIUrl":"10.1002/1873-3468.15052","url":null,"abstract":"<p>RNA is modified by &gt; 170 chemical modifications that affect its structure and function. Accordingly, RNA modifications have been implicated in regulation of gene expression and cellular outcomes in a variety of species spanning the phylogenetic tree. The study of RNA modifications is accelerated by generation of high-throughput methods for detecting RNA modifications at single base resolution. Here, we review recent advancement in next generation sequencing based approaches for detection of 14 distinct RNA modifications present in rRNA, tRNA and mRNA. We further outline the molecular and computational principles underlying currently available methods.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 1","pages":"19-32"},"PeriodicalIF":3.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 guide for blood–brain barrier models 血脑屏障模型指南
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-12 DOI: 10.1002/1873-3468.15053
Yomna Soliman, Jana Al-khodor, Gülnaz Yildirim Köken, Nur Mustafaoglu
{"title":"A guide for blood–brain barrier models","authors":"Yomna Soliman,&nbsp;Jana Al-khodor,&nbsp;Gülnaz Yildirim Köken,&nbsp;Nur Mustafaoglu","doi":"10.1002/1873-3468.15053","DOIUrl":"10.1002/1873-3468.15053","url":null,"abstract":"<p>Understanding the intricate mechanisms underlying brain-related diseases hinges on unraveling the pivotal role of the blood–brain barrier (BBB), an essential dynamic interface crucial for maintaining brain equilibrium. This review offers a comprehensive analysis of BBB physiology, delving into its cellular and molecular components while exploring a wide range of <i>in vivo</i> and <i>in vitro</i> BBB models. Notably, recent advancements in 3D cell culture techniques are explicitly discussed, as they have significantly improved the fidelity of BBB modeling by enabling the replication of physiologically relevant environments under flow conditions. Special attention is given to the cellular aspects of <i>in vitro</i> BBB models, alongside discussions on advances in stem cell technologies, providing valuable insights into generating robust cellular systems for BBB modeling. The diverse array of cell types used in BBB modeling, depending on their sources, is meticulously examined in this comprehensive review, scrutinizing their respective derivation protocols and implications. By synthesizing diverse approaches, this review sheds light on the improvements of BBB models to capture physiological conditions, aiding in understanding BBB interactions in health and disease conditions to foster clinical developments.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 5","pages":"599-644"},"PeriodicalIF":3.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
FoxO1 signaling in B cell malignancies and its therapeutic targeting. B 细胞恶性肿瘤中的 FoxO1 信号转导及其治疗靶点。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-12 DOI: 10.1002/1873-3468.15057
Krystof Hlavac, Petra Pavelkova, Laura Ondrisova, Marek Mraz
{"title":"FoxO1 signaling in B cell malignancies and its therapeutic targeting.","authors":"Krystof Hlavac, Petra Pavelkova, Laura Ondrisova, Marek Mraz","doi":"10.1002/1873-3468.15057","DOIUrl":"https://doi.org/10.1002/1873-3468.15057","url":null,"abstract":"<p><p>FoxO transcription factors (FoxO1, FoxO3a, FoxO4, FoxO6) are a highly evolutionary conserved subfamily of the 'forkhead' box proteins. They have traditionally been considered tumor suppressors, but FoxO1 also exhibits oncogenic properties. The complex nature of FoxO1 is illustrated by its various roles in B cell development and differentiation, immunoglobulin gene rearrangement and cell-surface B cell receptor (BCR) structure, DNA damage control, cell cycle regulation, and germinal center reaction. FoxO1 is tightly regulated at a transcriptional (STAT3, HEB, EBF, FoxOs) and post-transcriptional level (Akt, AMPK, CDK2, GSK3, IKKs, JNK, MAPK/Erk, SGK1, miRNA). In B cell malignancies, recurrent FoxO1 activating mutations (S22/T24) and aberrant nuclear export and activity have been described, underscoring the potential of its therapeutic inhibition. Here, we review FoxO1's roles across B cell and myeloid malignancies, namely acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), diffuse large B cell lymphoma (DLBCL), mantle cell lymphoma (MCL), Burkitt lymphoma (BL), Hodgkin lymphoma (HL), and multiple myeloma (MM). We also discuss preclinical evidence for FoxO1 targeting by currently available inhibitors (AS1708727, AS1842856, cpd10).</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Glu592 of the axon guidance receptor ROBO3 mediates a pH-dependent interaction with NELL2 ligand 轴突导向受体 ROBO3 的 Glu592 介导了与 NELL2 配体的 pH 依赖性相互作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-12 DOI: 10.1002/1873-3468.15054
Kimihiko Mizutani, Mayuko Toyoda, Teruyo Ojima-Kato, Andrés D. Maturana, Tomoaki Niimi
{"title":"Glu592 of the axon guidance receptor ROBO3 mediates a pH-dependent interaction with NELL2 ligand","authors":"Kimihiko Mizutani,&nbsp;Mayuko Toyoda,&nbsp;Teruyo Ojima-Kato,&nbsp;Andrés D. Maturana,&nbsp;Tomoaki Niimi","doi":"10.1002/1873-3468.15054","DOIUrl":"10.1002/1873-3468.15054","url":null,"abstract":"<p>There are only a few studies on the function of neuronal axon guidance molecules during low brain pH conditions. We previously reported that roundabout (ROBO) 2, a receptor for the axon guidance molecule SLIT, can bind to the neural epidermal growth factor-like-like (NELL) ligands in acidic conditions by conformational change of its ectodomain. Here, we show that the ROBO3 receptor also exhibits a pH-dependent increase in binding to the NELL2 ligand. We found that the Glu592 residue of ROBO3 at the binding interface between NELL2 and ROBO3 is a pH sensor and that the formation of a new hydrogen bonding network, due to protonation of the Glu592, leads to increased binding in acidic conditions. These results suggest that NELL2–ROBO3 signaling could be regulated by extracellular pH.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"571-580"},"PeriodicalIF":3.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Cordycepin generally inhibits growth factor signal transduction in a systems pharmacology study 在一项系统药理学研究中，虫草素通常会抑制生长因子信号转导。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-07 DOI: 10.1002/1873-3468.15046
Steven Lawrence, Jialiang Lin, Asma Khurshid, Wahyu Utami, Richa Singhania, Sadaf Ashraf, Graeme J. Thorn, Irengbam Rocky Mangangcha, Keith Spriggs, Dong-Hyun Kim, David Barrett, Cornelia H. de Moor
{"title":"Cordycepin generally inhibits growth factor signal transduction in a systems pharmacology study","authors":"Steven Lawrence,&nbsp;Jialiang Lin,&nbsp;Asma Khurshid,&nbsp;Wahyu Utami,&nbsp;Richa Singhania,&nbsp;Sadaf Ashraf,&nbsp;Graeme J. Thorn,&nbsp;Irengbam Rocky Mangangcha,&nbsp;Keith Spriggs,&nbsp;Dong-Hyun Kim,&nbsp;David Barrett,&nbsp;Cornelia H. de Moor","doi":"10.1002/1873-3468.15046","DOIUrl":"10.1002/1873-3468.15046","url":null,"abstract":"<p>Cordycepin (3′ deoxyadenosine) has been widely researched as a potential cancer therapy, but many diverse mechanisms of action have been proposed. Here, we confirm that cordycepin triphosphate is likely to be the active metabolite of cordycepin and that it consistently represses growth factor-induced gene expression. Bioinformatic analysis, quantitative PCR and western blotting confirmed that cordycepin blocks the PI3K/AKT/mTOR and/or MEK/ERK pathways in six cell lines and that AMPK activation is not required. The effects of cordycepin on translation through mTOR pathway repression were detectable within 30 min, indicating a rapid process. These data therefore indicate that cordycepin has a universal mechanism of action, acting as cordycepin triphosphate on an as yet unknown target molecule involved in growth factor signalling.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 3","pages":"415-435"},"PeriodicalIF":3.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Cryo-EM structure of a novel α-synuclein filament subtype from multiple system atrophy 多系统萎缩症中一种新型α-突触核蛋白丝亚型的冷冻电子显微镜结构。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-07 DOI: 10.1002/1873-3468.15048
Nicholas L. Yan, Francisco Candido, Eric Tse, Arthur A. Melo, Stanley B. Prusiner, Daniel A. Mordes, Daniel R. Southworth, Nick A. Paras, Gregory E. Merz
{"title":"Cryo-EM structure of a novel α-synuclein filament subtype from multiple system atrophy","authors":"Nicholas L. Yan,&nbsp;Francisco Candido,&nbsp;Eric Tse,&nbsp;Arthur A. Melo,&nbsp;Stanley B. Prusiner,&nbsp;Daniel A. Mordes,&nbsp;Daniel R. Southworth,&nbsp;Nick A. Paras,&nbsp;Gregory E. Merz","doi":"10.1002/1873-3468.15048","DOIUrl":"10.1002/1873-3468.15048","url":null,"abstract":"<p>Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by accumulation of α-synuclein cross-β amyloid filaments in the brain. Previous structural studies of these filaments by cryo-electron microscopy (cryo-EM) revealed three discrete folds distinct from α-synuclein filaments associated with other neurodegenerative diseases. Here, we use cryo-EM to identify a novel, low-populated MSA filament subtype (designated Type I<sub>2</sub>) in addition to a predominant class comprising MSA Type II<sub>2</sub> filaments. The 3.3-Å resolution structure of the Type I<sub>2</sub> filament reveals a fold consisting of two asymmetric protofilaments, one of which adopts a novel structure that is chimeric between two previously reported protofilaments. These results further define MSA-specific folds of α-synuclein filaments and have implications for designing MSA diagnostics and therapeutics.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 1","pages":"33-40"},"PeriodicalIF":3.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
14-3-3ε conditional knockout mice exhibit defects in the development of the epidermis 14-3-3ε 条件性基因敲除小鼠表现出表皮发育缺陷。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-11-07 DOI: 10.1002/1873-3468.15051
Sarika Tilwani, Karan Gandhi, Sorab N. Dalal
{"title":"14-3-3ε conditional knockout mice exhibit defects in the development of the epidermis","authors":"Sarika Tilwani,&nbsp;Karan Gandhi,&nbsp;Sorab N. Dalal","doi":"10.1002/1873-3468.15051","DOIUrl":"10.1002/1873-3468.15051","url":null,"abstract":"<p>The epidermis is a stratified epithelium that functions as the first line of defense against pathogenic invasion and acts as a barrier preventing water loss. In this study, we aimed to decipher the role of 14-3-3ε in the development of the epidermis. We report that loss of 14-3-3ε in the epidermis of juvenile and adult mice reduces cell division in the basal layer and increases the percentage of cells with multiple centrosomes, leading to a reduction in the thickness of the basal and stratified layers. We also demonstrate a decrease in the expression of differentiation markers, although no gross morphological defects in the skin or adverse effects on the survival of the mice were observed. These results suggest that loss of 14-3-3ε in the epidermis may lead to defects in proliferation and differentiation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 24","pages":"3005-3020"},"PeriodicalIF":3.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11666074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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