Journal of cell science最新文献_第9页

N-terminal tags impair the ability of lamin A to provide structural support to the nucleus. N 端标签会削弱 Lamin A 为细胞核提供结构支持的能力。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-23 DOI: 10.1242/jcs.262207

Jacob Odell, Jan Lammerding

{"title":"N-terminal tags impair the ability of lamin A to provide structural support to the nucleus.","authors":"Jacob Odell, Jan Lammerding","doi":"10.1242/jcs.262207","DOIUrl":"10.1242/jcs.262207","url":null,"abstract":"Lamins are intermediate filament proteins that contribute to numerous cellular functions, including nuclear morphology and mechanical stability. The N-terminal head domain of lamin is crucial for higher order filament assembly and function, yet the effects of commonly used N-terminal tags on lamin function remain largely unexplored. Here, we systematically studied the effect of two differently sized tags on lamin A (LaA) function in a mammalian cell model engineered to allow for precise control of expression of tagged lamin proteins. Untagged, FLAG-tagged and GFP-tagged LaA completely rescued nuclear shape defects when expressed at similar levels in lamin A/C-deficient (Lmna-/-) MEFs, and all LaA constructs prevented increased nuclear envelope ruptures in these cells. N-terminal tags, however, altered the nuclear localization of LaA and impaired the ability of LaA to restore nuclear deformability and to recruit emerin to the nuclear membrane in Lmna-/- MEFs. Our finding that tags impede some LaA functions but not others might explain the partial loss of function phenotypes when tagged lamins are expressed in model organisms and should caution researchers using tagged lamins to study the nucleus.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

When less is more - a fast TurboID knock-in approach for high-sensitivity endogenous interactome mapping. 少即是多--高灵敏度内源性相互作用组图谱的快速 TurboID KI 方法。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-28 DOI: 10.1242/jcs.261952

Alexander Stockhammer, Carissa Spalt, Antonia Klemt, Laila S Benz, Shelly Harel, Vini Natalia, Lukas Wiench, Christian Freund, Benno Kuropka, Francesca Bottanelli

{"title":"When less is more - a fast TurboID knock-in approach for high-sensitivity endogenous interactome mapping.","authors":"Alexander Stockhammer, Carissa Spalt, Antonia Klemt, Laila S Benz, Shelly Harel, Vini Natalia, Lukas Wiench, Christian Freund, Benno Kuropka, Francesca Bottanelli","doi":"10.1242/jcs.261952","DOIUrl":"10.1242/jcs.261952","url":null,"abstract":"In recent years, proximity labeling has established itself as an unbiased and powerful approach to map the interactome of specific proteins. Although physiological expression of labeling enzymes is beneficial for the mapping of interactors, generation of the desired cell lines remains time-consuming and challenging. Using our established pipeline for rapid generation of C- and N-terminal CRISPR-Cas9 knock-ins (KIs) based on antibiotic selection, we were able to compare the performance of commonly used labeling enzymes when endogenously expressed. Endogenous tagging of the µ subunit of the adaptor protein (AP)-1 complex with TurboID allowed identification of known interactors and cargo proteins that simple overexpression of a labeling enzyme fusion protein could not reveal. We used the KI strategy to compare the interactome of the different AP complexes and clathrin and were able to assemble lists of potential interactors and cargo proteins that are specific for each sorting pathway. Our approach greatly simplifies the execution of proximity labeling experiments for proteins in their native cellular environment and allows going from CRISPR transfection to mass spectrometry analysis and interactome data in just over a month.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Mechanistic divergences of endocytic clathrin-coated vesicle formation in mammals, yeasts and plants. 哺乳动物、酵母和植物内凝集素包囊形成的机制差异

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-20 DOI: 10.1242/jcs.261847

Alexander Johnson

{"title":"Mechanistic divergences of endocytic clathrin-coated vesicle formation in mammals, yeasts and plants.","authors":"Alexander Johnson","doi":"10.1242/jcs.261847","DOIUrl":"10.1242/jcs.261847","url":null,"abstract":"Clathrin-coated vesicles (CCVs), generated by clathrin-mediated endocytosis (CME), are essential eukaryotic trafficking organelles that transport extracellular and plasma membrane-bound materials into the cell. In this Review, we explore mechanisms of CME in mammals, yeasts and plants, and highlight recent advances in the characterization of endocytosis in plants. Plants separated from mammals and yeast over 1.5 billion years ago, and plant cells have distinct biophysical parameters that can influence CME, such as extreme turgor pressure. Plants can therefore provide a wider perspective on fundamental processes in eukaryotic cells. We compare key mechanisms that drive CCV formation and explore what these mechanisms might reveal about the core principles of endocytosis across the tree of life. Fascinatingly, CME in plants appears to more closely resemble that in mammalian cells than that in yeasts, despite plants being evolutionarily further from mammals than yeast. Endocytic initiation appears to be highly conserved across these three systems, requiring similar protein domains and regulatory processes. Clathrin coat proteins and their honeycomb lattice structures are also highly conserved. However, major differences are found in membrane-bending mechanisms. Unlike in mammals or yeast, plant endocytosis occurs independently of actin, highlighting that mechanistic assumptions about CME across different systems should be made with caution.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142004325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Excess microtubule and F-actin formation mediates shortening and loss of primary cilia in response to a hyperosmotic milieu. 微管和 F-肌动蛋白的过度形成介导了初级纤毛在高渗透环境下的缩短和脱落。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-30 DOI: 10.1242/jcs.261988

Hiroshi Otani, Ryota Nakazato, Kanae Koike, Keisuke Ohta, Koji Ikegami

{"title":"Excess microtubule and F-actin formation mediates shortening and loss of primary cilia in response to a hyperosmotic milieu.","authors":"Hiroshi Otani, Ryota Nakazato, Kanae Koike, Keisuke Ohta, Koji Ikegami","doi":"10.1242/jcs.261988","DOIUrl":"10.1242/jcs.261988","url":null,"abstract":"The primary cilium is a small organelle protruding from the cell surface that receives signals from the extracellular milieu. Although dozens of studies have reported that several genetic factors can impair the structure of primary cilia, evidence for environmental stimuli affecting primary cilia structures is limited. Here, we investigated an extracellular stress that affected primary cilia morphology and its underlying mechanisms. Hyperosmotic shock induced reversible shortening and disassembly of the primary cilia of murine intramedullary collecting duct cells. The shortening of primary cilia caused by hyperosmotic shock followed delocalization of the pericentriolar material (PCM). Excessive microtubule and F-actin formation in the cytoplasm coincided with the hyperosmotic shock-induced changes to primary cilia and the PCM. Treatment with a microtubule-disrupting agent, nocodazole, partially prevented the hyperosmotic shock-induced disassembly of primary cilia and almost completely prevented delocalization of the PCM. An actin polymerization inhibitor, latrunculin A, also partially prevented the hyperosmotic shock-induced shortening and disassembly of primary cilia and almost completely prevented delocalization of the PCM. We demonstrate that hyperosmotic shock induces reversible morphological changes in primary cilia and the PCM in a manner dependent on excessive formation of microtubule and F-actin.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Two paralogous PHD finger proteins participate in natural genome editing in Paramecium tetraurelia. 两个同源的 PHD 手指蛋白参与了四膜虫的天然基因组编辑。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-30 DOI: 10.1242/jcs.261979

Lilia Häußermann, Aditi Singh, Estienne C Swart

{"title":"Two paralogous PHD finger proteins participate in natural genome editing in Paramecium tetraurelia.","authors":"Lilia Häußermann, Aditi Singh, Estienne C Swart","doi":"10.1242/jcs.261979","DOIUrl":"10.1242/jcs.261979","url":null,"abstract":"The unicellular eukaryote Paramecium tetraurelia contains functionally distinct nuclei: germline micronuclei (MICs) and a somatic macronucleus (MAC). During sex, the MIC genome is reorganized into a new MAC genome and the old MAC is lost. Almost 45,000 unique internal eliminated sequences (IESs) distributed throughout the genome require precise excision to guarantee a functional new MAC genome. Here, we characterize a pair of paralogous PHD finger proteins involved in DNA elimination. DevPF1, the early-expressed paralog, is present in only some of the gametic and post-zygotic nuclei during meiosis. Both DevPF1 and DevPF2 localize in the new developing MACs, where IES excision occurs. Upon DevPF2 knockdown (KD), long IESs are preferentially retained and late-expressed small RNAs decrease; no length preference for retained IESs was observed in DevPF1-KD and development-specific small RNAs were abolished. The expression of at least two genes from the new MAC with roles in genome reorganization seems to be influenced by DevPF1- and DevPF2-KD. Thus, both PHD fingers are crucial for new MAC genome development, with distinct functions, potentially via regulation of non-coding and coding transcription in the MICs and new MACs.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Hominini-specific regulation of the cell cycle by stop codon readthrough of FEM1B. FEM1B的终止密码子通读对细胞周期的特异性调控。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-29 DOI: 10.1242/jcs.261921

Md Noor Akhtar, Anumeha Singh, Lekha E Manjunath, Dhruba Dey, Sangeetha Devi Kumar, Kirtana Vasu, Arpan Das, Sandeep M Eswarappa

{"title":"Hominini-specific regulation of the cell cycle by stop codon readthrough of FEM1B.","authors":"Md Noor Akhtar, Anumeha Singh, Lekha E Manjunath, Dhruba Dey, Sangeetha Devi Kumar, Kirtana Vasu, Arpan Das, Sandeep M Eswarappa","doi":"10.1242/jcs.261921","DOIUrl":"10.1242/jcs.261921","url":null,"abstract":"FEM1B is a substrate-recognition component of the CRL2 E3 ubiquitin-protein ligase. This multi-protein complex targets specific proteins for ubiquitylation, which leads to their degradation. Here, we demonstrate the regulation of FEM1B expression by stop codon readthrough (SCR). In this process, translating ribosomes readthrough the stop codon of FEM1B to generate a C-terminally extended isoform that is highly unstable. A total of 81 nucleotides in the proximal 3'UTR of FEM1B constitute the necessary and sufficient cis-signal for SCR. Also, they encode the amino acid sequence responsible for the degradation of the SCR product. CRISPR-edited cells lacking this region, and therefore SCR of FEM1B, showed increased FEM1B expression. This in turn resulted in reduced expression of SLBP (a target of FEM1B-mediated degradation) and replication-dependent histones (target of SLBP for mRNA stability), causing cell cycle delay. Evolutionary analysis revealed that this phenomenon is specific to the genus Pan and Homo (Hominini). Overall, we show a relatively recently evolved SCR process that relieves the cell cycle from the negative regulation by FEM1B.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Reprogramming macrophages with R848-loaded artificial protocells to modulate skin and skeletal wound healing. 用负载 R848 的人工原细胞重编程巨噬细胞，以调节皮肤和骨骼伤口愈合。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-29 DOI: 10.1242/jcs.262202

Paco López-Cuevas, Tiah C L Oates, Qiao Tong, Lucy M McGowan, Stephen J Cross, Can Xu, Yu Zhao, Zhuping Yin, Ashley M Toye, Asme Boussahel, Chrissy L Hammond, Stephen Mann, Paul Martin

{"title":"Reprogramming macrophages with R848-loaded artificial protocells to modulate skin and skeletal wound healing.","authors":"Paco López-Cuevas, Tiah C L Oates, Qiao Tong, Lucy M McGowan, Stephen J Cross, Can Xu, Yu Zhao, Zhuping Yin, Ashley M Toye, Asme Boussahel, Chrissy L Hammond, Stephen Mann, Paul Martin","doi":"10.1242/jcs.262202","DOIUrl":"10.1242/jcs.262202","url":null,"abstract":"After tissue injury, inflammatory cells are rapidly recruited to the wound where they clear microbes and other debris, and coordinate the behaviour of other cell lineages at the repair site in both positive and negative ways. In this study, we take advantage of the translucency and genetic tractability of zebrafish to evaluate the feasibility of reprogramming innate immune cells in vivo with cargo-loaded protocells and investigate how this alters the inflammatory response in the context of skin and skeletal repair. Using live imaging, we show that protocells loaded with R848 cargo (which targets TLR7 and TLR8 signalling), are engulfed by macrophages resulting in their switching to a pro-inflammatory phenotype and altering their regulation of angiogenesis, collagen deposition and re-epithelialization during skin wound healing, as well as dampening osteoblast and osteoclast recruitment and bone mineralization during fracture repair. For infected skin wounds, R848-reprogrammed macrophages exhibited enhanced bactericidal activities leading to improved healing. We replicated our zebrafish studies in cultured human macrophages, and showed that R848-loaded protocells similarly reprogramme human cells, indicating how this strategy might be used to modulate wound inflammation in the clinic.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

MYCBPAP is a central apparatus protein required for centrosome-nuclear envelope docking and sperm tail biogenesis in mice. MYCBPAP 是小鼠中心体-核包膜对接和精子尾部生物生成所需的中心器蛋白。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-15 Epub Date: 2024-08-29 DOI: 10.1242/jcs.261962

Haoting Wang, Hiroko Kobayashi, Keisuke Shimada, Seiya Oura, Yuki Oyama, Hiroaki Kitakaze, Taichi Noda, Norikazu Yabuta, Haruhiko Miyata, Masahito Ikawa

{"title":"MYCBPAP is a central apparatus protein required for centrosome-nuclear envelope docking and sperm tail biogenesis in mice.","authors":"Haoting Wang, Hiroko Kobayashi, Keisuke Shimada, Seiya Oura, Yuki Oyama, Hiroaki Kitakaze, Taichi Noda, Norikazu Yabuta, Haruhiko Miyata, Masahito Ikawa","doi":"10.1242/jcs.261962","DOIUrl":"10.1242/jcs.261962","url":null,"abstract":"The structure of the sperm flagellar axoneme is highly conserved across species and serves the essential function of generating motility to facilitate the meeting of spermatozoa with the egg. During spermiogenesis, the axoneme elongates from the centrosome, and subsequently the centrosome docks onto the nuclear envelope to continue tail biogenesis. Mycbpap is expressed predominantly in mouse and human testes and conserved in Chlamydomonas as FAP147. A previous cryo-electron microscopy analysis has revealed the localization of FAP147 to the central apparatus of the axoneme. Here, we generated Mycbpap-knockout mice and demonstrated the essential role of Mycbpap in male fertility. Deletion of Mycbpap led to disrupted centrosome-nuclear envelope docking and abnormal flagellar biogenesis. Furthermore, we generated transgenic mice with tagged MYCBPAP, which restored the fertility of Mycbpap-knockout males. Interactome analyses of MYCBPAP using Mycbpap transgenic mice unveiled binding partners of MYCBPAP including central apparatus proteins, such as CFAP65 and CFAP70, which constitute the C2a projection, and centrosome-associated proteins, such as CCP110. These findings provide insights into a MYCBPAP-dependent regulation of the centrosome-nuclear envelope docking and sperm tail biogenesis.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11385322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

First person – Jiwon Lee 第一人 - Jiwon Lee

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-08 DOI: 10.1242/jcs.263427

引用次数: 0

Conjugation of ATG8s to single membranes at a glance. ATG8s 与单层膜的共轭情况一览。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-08-01 Epub Date: 2024-08-15 DOI: 10.1242/jcs.261031

Carmen Figueras-Novoa, Lewis Timimi, Elena Marcassa, Rachel Ulferts, Rupert Beale

{"title":"Conjugation of ATG8s to single membranes at a glance.","authors":"Carmen Figueras-Novoa, Lewis Timimi, Elena Marcassa, Rachel Ulferts, Rupert Beale","doi":"10.1242/jcs.261031","DOIUrl":"10.1242/jcs.261031","url":null,"abstract":"Autophagy refers to a set of degradative mechanisms whereby cytoplasmic contents are targeted to the lysosome. This is best described for macroautophagy, where a double-membrane compartment (autophagosome) is generated to engulf cytoplasmic contents. Autophagosomes are decorated with ubiquitin-like ATG8 molecules (ATG8s), which are recruited through covalent lipidation, catalysed by the E3-ligase-like ATG16L1 complex. LC3 proteins are ATG8 family members that are often used as a marker for autophagosomes. In contrast to canonical macroautophagy, conjugation of ATG8s to single membranes (CASM) describes a group of non-canonical autophagy processes in which ATG8s are targeted to pre-existing single-membrane compartments. CASM occurs in response to disrupted intracellular pH gradients, when the V-ATPase proton pump recruits ATG16L1 in a process called V-ATPase-ATG16L1-induced LC3 lipidation (VAIL). Recent work has demonstrated a parallel, alternative axis for CASM induction, triggered when the membrane recruitment factor TECPR1 recognises sphingomyelin exposed on the cytosolic face of a membrane and forms an alternative E3-ligase-like complex. This sphingomyelin-TECPR1-induced LC3 lipidation (STIL) is independent of the V-ATPase and ATG16L1. In light of these discoveries, this Cell Science at a Glance article summarises these two mechanisms of CASM to highlight how they differ from canonical macroautophagy, and from each other.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141982352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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