Nucleus (Austin, Tex.)最新文献

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The nuclear envelope in higher plant mitosis and meiosis. 高等植物有丝分裂和减数分裂中的核膜。
Nucleus (Austin, Tex.) Pub Date : 2019-12-01 Epub Date: 2019-03-17 DOI: 10.1080/19491034.2019.1587277
Monica Pradillo, David Evans, Katja Graumann
{"title":"The nuclear envelope in higher plant mitosis and meiosis.","authors":"Monica Pradillo,&nbsp;David Evans,&nbsp;Katja Graumann","doi":"10.1080/19491034.2019.1587277","DOIUrl":"10.1080/19491034.2019.1587277","url":null,"abstract":"<p><p>Mitosis and meiosis in higher plants involve significant reconfiguration of the nuclear envelope and the proteins that interact with it. The dynamic series of events involves a range of interactions, movement, breakdown, and reformation of this complex system. Recently, progress has been made in identifying and characterizing the protein and membrane interactome that performs these complex tasks, including constituents of the nuclear envelope, the cytoskeleton, nucleoskeleton, and chromatin. This review will present the current understanding of these interactions and advances in knowledge of the processes for the breakdown and reformation of the nuclear envelope during cell divisions in plants.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2019.1587277","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37224754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 16
Interplay of lamin A and lamin B LADs on the radial positioning of chromatin. 纤层蛋白A和纤层蛋白B在染色质径向定位中的相互作用。
Nucleus (Austin, Tex.) Pub Date : 2019-12-01 DOI: 10.1080/19491034.2019.1570810
Frida Forsberg, Annaël Brunet, Tharvesh M Liyakat Ali, Philippe Collas
{"title":"Interplay of lamin A and lamin B LADs on the radial positioning of chromatin.","authors":"Frida Forsberg,&nbsp;Annaël Brunet,&nbsp;Tharvesh M Liyakat Ali,&nbsp;Philippe Collas","doi":"10.1080/19491034.2019.1570810","DOIUrl":"https://doi.org/10.1080/19491034.2019.1570810","url":null,"abstract":"<p><p>Immunosuppressive drugs such as cyclosporin A (CsA) can elicit hepatotoxicity by affecting gene expression. Here, we address the link between CsA and large-scale chromatin organization in HepG2 hepatocarcinoma cells. We show the existence of lamina-associated domains (LADs) interacting with lamin A, lamin B, or both. These 'A-B', 'A-only' and 'B-only' LADs display distinct fates after CsA treatment: A-B LADs remain constitutive or lose A, A-only LADs mainly lose A or switch to B, and B-only LADs remain B-only or acquire A. LAD rearrangement is overall uncoupled from changes in gene expression. Three-dimensional (3D) genome modeling predicts changes in radial positioning of LADs as LADs switch identities, which are corroborated by fluorescence in situ hybridization. Our results reveal interplay between A- and B-type lamins on radial locus positioning, suggesting complementary contributions to large-scale genome architecture. The data also unveil a hitherto unsuspected impact of cytotoxic drugs on genome conformation.Abbreviations: ChIP-seq: chromatin immunoprecipitation sequencing; CsA: cyclosporin A; FISH; fluorescence in situ hybridization; ICMT: isoprenylcysteine methyltransferase; LAD: lamina-associated domain; TAD: topologically-associated domain.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2019.1570810","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36871387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 26
ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres. ALT控制,删除:FANCM作为端粒选择性延长的抗癌靶点。
Nucleus (Austin, Tex.) Pub Date : 2019-12-01 DOI: 10.1080/19491034.2019.1685246
Julienne J O'Rourke, Rohan Bythell-Douglas, Elyse A Dunn, Andrew J Deans
{"title":"ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres.","authors":"Julienne J O'Rourke,&nbsp;Rohan Bythell-Douglas,&nbsp;Elyse A Dunn,&nbsp;Andrew J Deans","doi":"10.1080/19491034.2019.1685246","DOIUrl":"https://doi.org/10.1080/19491034.2019.1685246","url":null,"abstract":"<p><p>Break-induced replication is a specific type of DNA repair that has a co-opted role in telomere extension by telomerase-negative cancer cells. This Alternative Lengthening of Telomeres (or 'ALT') is required for viability in approximately 10% of all carcinomas, but up to 50% of the soft-tissue derived sarcomas. In several recent studies, we and others demonstrate that expression and activity of FANCM, a DNA translocase protein, is essential for the viability of ALT-associated cancers. Here we provide a summary of how and why FANCM depletion leads to deletion of ALT-controlled cancers, predominantly through a hyper-activation of break-induced replication. We also discuss how FANCM can and has been targeted in cancer cell killing, including potential opportunities in ALT and other genetic backgrounds.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2019.1685246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40452800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 13
Plant condensin II is required for the correct spatial relationship between centromeres and rDNA arrays. 植物凝聚素II是着丝粒和rDNA阵列之间正确的空间关系所必需的。
Nucleus (Austin, Tex.) Pub Date : 2019-12-01 DOI: 10.1080/19491034.2019.1616507
Takuya Sakamoto, Tomoya Sugiyama, Tomoe Yamashita, Sachihiro Matsunaga
{"title":"Plant condensin II is required for the correct spatial relationship between centromeres and rDNA arrays.","authors":"Takuya Sakamoto,&nbsp;Tomoya Sugiyama,&nbsp;Tomoe Yamashita,&nbsp;Sachihiro Matsunaga","doi":"10.1080/19491034.2019.1616507","DOIUrl":"https://doi.org/10.1080/19491034.2019.1616507","url":null,"abstract":"<p><p>Plants possess the structural maintenance of chromosome (SMC) protein complexes cohesin, condensin, and SMC5/6, which function in fundamental biological processes such as sister chromatid cohesion, chromosome condensation and segregation, and damaged DNA repair. Recently, increasing evidence in several organisms has suggested that condensin is involved in chromatin organizations during interphase. In Arabidopsis thaliana, condensin II is localized in the nucleus throughout interphase and is suggested to be required for keeping centromeres apart and the assembly of euchromatic chromosome arms. However, it remains unclear how condensin II organizes chromatin associations. Here, we first showed the high possibility that the function of condensin II as a complex is required for the disassociation of centromeres. Analysis of the rDNA array distribution revealed that condensin II is also indispensable for the association of centromeres with rDNA arrays. Reduced axial compaction of chromosomes and impaired genome integrity in condensin II mutants are not related to the disruption of chromatin organization. In contrast, the axial compaction of chromosomes by condensin II produces the force leading to the disassociation of heterologous centromeres in Drosophila melanogaster. Taken together, our data imply that the condensin II function in chromatin organization differs among eukaryotes.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2019.1616507","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37241383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
Comprehensive nuclear proteome of Arabidopsis obtained by sequential extraction. 序列提取法获得拟南芥核蛋白质组。
Nucleus (Austin, Tex.) Pub Date : 2019-12-01 DOI: 10.1080/19491034.2019.1603093
Chieko Goto, Shoko Hashizume, Yoichiro Fukao, Ikuko Hara-Nishimura, Kentaro Tamura
{"title":"Comprehensive nuclear proteome of Arabidopsis obtained by sequential extraction.","authors":"Chieko Goto,&nbsp;Shoko Hashizume,&nbsp;Yoichiro Fukao,&nbsp;Ikuko Hara-Nishimura,&nbsp;Kentaro Tamura","doi":"10.1080/19491034.2019.1603093","DOIUrl":"https://doi.org/10.1080/19491034.2019.1603093","url":null,"abstract":"<p><p>In eukaryotes, the nucleus plays key roles in fundamental cellular processes, including DNA replication, chromatin maintenance, transcription, and translation. To better understand the functional diversity of nuclei, we developed a method for the comprehensive extraction of the nuclear proteome from Arabidopsis. We used a buffer with a high sucrose concentration to purify nuclei and then conducted solubility-based fractionation to increase proteome coverage. We identified 1539 proteins and two novel nuclear envelope (NE) proteins in the nuclear fraction of Arabidopsis cultured cells. The localization of 25 proteins was determined by GFP fusion analyses; 23 of these proteins were localized either in the nucleus or the NE-associated endoplasmic reticulum. This result was indicative of the high quality of the proteome. These findings will be useful for clarifying novel nuclear functions in plants.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2019.1603093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37133852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 22
Genomic instability and DNA replication defects in progeroid syndromes. 类早衰综合征的基因组不稳定性和DNA复制缺陷。
Nucleus (Austin, Tex.) Pub Date : 2018-12-31 Epub Date: 2018-06-23 DOI: 10.1080/19491034.2018.1476793
Romina Burla, Mattia La Torre, Chiara Merigliano, Fiammetta Vernì, Isabella Saggio
{"title":"Genomic instability and DNA replication defects in progeroid syndromes.","authors":"Romina Burla,&nbsp;Mattia La Torre,&nbsp;Chiara Merigliano,&nbsp;Fiammetta Vernì,&nbsp;Isabella Saggio","doi":"10.1080/19491034.2018.1476793","DOIUrl":"https://doi.org/10.1080/19491034.2018.1476793","url":null,"abstract":"<p><p>Progeroid syndromes induced by mutations in lamin A or in its interactors - named progeroid laminopathies - are model systems for the dissection of the molecular pathways causing physiological and premature aging. A large amount of data, based mainly on the Hutchinson Gilford Progeria syndrome (HGPS), one of the best characterized progeroid laminopathy, has highlighted the role of lamins in multiple DNA activities, including replication, repair, chromatin organization and telomere function. On the other hand, the phenotypes generated by mutations affecting genes directly acting on DNA function, as mutations in the helicases WRN and BLM or in the polymerase polδ, share many of the traits of progeroid laminopathies. These evidences support the hypothesis of a concerted implication of DNA function and lamins in aging. We focus here on these aspects to contribute to the comprehension of the driving forces acting in progeroid syndromes and premature aging.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2018.1476793","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36252459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 36
Progerin phosphorylation in interphase is lower and less mechanosensitive than lamin-A,C in iPS-derived mesenchymal stem cells. 在ips来源的间充质干细胞中,间期的Progerin磷酸化比lamin-A,C更低,机械敏感性更低。
Nucleus (Austin, Tex.) Pub Date : 2018-01-01 DOI: 10.1080/19491034.2018.1460185
Sangkyun Cho, Amal Abbas, Jerome Irianto, Irena L Ivanovska, Yuntao Xia, Manu Tewari, Dennis E Discher
{"title":"Progerin phosphorylation in interphase is lower and less mechanosensitive than lamin-A,C in iPS-derived mesenchymal stem cells.","authors":"Sangkyun Cho,&nbsp;Amal Abbas,&nbsp;Jerome Irianto,&nbsp;Irena L Ivanovska,&nbsp;Yuntao Xia,&nbsp;Manu Tewari,&nbsp;Dennis E Discher","doi":"10.1080/19491034.2018.1460185","DOIUrl":"https://doi.org/10.1080/19491034.2018.1460185","url":null,"abstract":"<p><p>Interphase phosphorylation of lamin-A,C depends dynamically on a cell's microenvironment, including the stiffness of extracellular matrix. However, phosphorylation dynamics is poorly understood for diseased forms such as progerin, a permanently farnesylated mutant of LMNA that accelerates aging of stiff and mechanically stressed tissues. Here, fine-excision alignment mass spectrometry (FEA-MS) is developed to quantify progerin and its phosphorylation levels in patient iPS cells differentiated to mesenchymal stem cells (MSCs). The stoichiometry of total A-type lamins (including progerin) versus B-type lamins measured for Progeria iPS-MSCs prove similar to that of normal MSCs, with total A-type lamins more abundant than B-type lamins. However, progerin behaves more like farnesylated B-type lamins in mechanically-induced segregation from nuclear blebs. Phosphorylation of progerin at multiple sites in iPS-MSCs cultured on rigid plastic is also lower than that of normal lamin-A and C. Reduction of nuclear tension upon i) cell rounding/detachment from plastic, ii) culture on soft gels, and iii) inhibition of actomyosin stress increases phosphorylation and degradation of lamin-C > lamin-A > progerin. Such mechano-sensitivity diminishes, however, with passage as progerin and DNA damage accumulate. Lastly, transcription-regulating retinoids exert equal effects on both diseased and normal A-type lamins, suggesting a differential mechano-responsiveness might best explain the stiff tissue defects in Progeria.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2018.1460185","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10740693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 25
Uncovering mechanisms of nuclear degradation in keratinocytes: A paradigm for nuclear degradation in other tissues. 揭示角质形成细胞中核降解的机制:其他组织中核降解的范例。
Nucleus (Austin, Tex.) Pub Date : 2018-01-01 Epub Date: 2018-01-03 DOI: 10.1080/19491034.2017.1412027
Clare Rogerson, Daniele Bergamaschi, Ryan F L O'Shaughnessy
{"title":"Uncovering mechanisms of nuclear degradation in keratinocytes: A paradigm for nuclear degradation in other tissues.","authors":"Clare Rogerson,&nbsp;Daniele Bergamaschi,&nbsp;Ryan F L O'Shaughnessy","doi":"10.1080/19491034.2017.1412027","DOIUrl":"https://doi.org/10.1080/19491034.2017.1412027","url":null,"abstract":"<p><p>Eukaryotic nuclei are essential organelles, storing the majority of the cellular DNA, comprising the site of most DNA and RNA synthesis, controlling gene expression and therefore regulating cellular function. The majority of mammalian cells retain their nucleus throughout their lifetime, however, in three mammalian tissues the nucleus is entirely removed and its removal is essential for cell function. Lens fibre cells, erythroblasts and epidermal keratinocytes all lose their nucleus in the terminal differentiation pathways of these cell types. However, relatively little is known about the pathways that lead to complete nuclear removal and about how these pathways are regulated. In this review, we aim to discuss the current understanding of nuclear removal mechanisms in these three cell types and expand upon how recent studies into nuclear degradation in keratinocytes, an easily accessible experimental model, could contribute to a wider understanding of these molecular mechanisms in both health and pathology.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2017.1412027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35311503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 18
Extrusion without a motor: a new take on the loop extrusion model of genome organization. 无马达挤出:基因组组织环挤出模型的新进展。
Nucleus (Austin, Tex.) Pub Date : 2018-01-01 DOI: 10.1080/19491034.2017.1421825
C A Brackley, J Johnson, D Michieletto, A N Morozov, M Nicodemi, P R Cook, D Marenduzzo
{"title":"Extrusion without a motor: a new take on the loop extrusion model of genome organization.","authors":"C A Brackley,&nbsp;J Johnson,&nbsp;D Michieletto,&nbsp;A N Morozov,&nbsp;M Nicodemi,&nbsp;P R Cook,&nbsp;D Marenduzzo","doi":"10.1080/19491034.2017.1421825","DOIUrl":"https://doi.org/10.1080/19491034.2017.1421825","url":null,"abstract":"<p><p>Chromatin loop extrusion is a popular model for the formation of CTCF loops and topological domains. Recent HiC data have revealed a strong bias in favour of a particular arrangement of the CTCF binding motifs that stabilize loops, and extrusion is the only model to date which can explain this. However, the model requires a motor to generate the loops, and although cohesin is a strong candidate for the extruding factor, a suitable motor protein (or a motor activity in cohesin itself) has yet to be found. Here we explore a new hypothesis: that there is no motor, and thermal motion within the nucleus drives extrusion. Using theoretical modelling and computer simulations we ask whether such diffusive extrusion could feasibly generate loops. Our simulations uncover an interesting ratchet effect (where an osmotic pressure promotes loop growth), and suggest, by comparison to recent in vitro and in vivo measurements, that diffusive extrusion can in principle generate loops of the size observed in the data. Extra View on : C. A. Brackley, J. Johnson, D. Michieletto, A. N. Morozov, M. Nicodemi, P. R. Cook, and D. Marenduzzo \"Non-equilibrium chromosome looping via molecular slip-links\", Physical Review Letters 119 138101 (2017).</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2017.1421825","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35707134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 35
An overview of treatment strategies for Hutchinson-Gilford Progeria syndrome. 哈钦森-吉尔福德早衰综合征治疗策略综述。
Nucleus (Austin, Tex.) Pub Date : 2018-01-01 DOI: 10.1080/19491034.2018.1460045
Karim Harhouri, Diane Frankel, Catherine Bartoli, Patrice Roll, Annachiara De Sandre-Giovannoli, Nicolas Lévy
{"title":"An overview of treatment strategies for Hutchinson-Gilford Progeria syndrome.","authors":"Karim Harhouri,&nbsp;Diane Frankel,&nbsp;Catherine Bartoli,&nbsp;Patrice Roll,&nbsp;Annachiara De Sandre-Giovannoli,&nbsp;Nicolas Lévy","doi":"10.1080/19491034.2018.1460045","DOIUrl":"https://doi.org/10.1080/19491034.2018.1460045","url":null,"abstract":"<p><p>Hutchinson-Gilford progeria syndrome (HGPS) is a sporadic, autosomal dominant disorder characterized by premature and accelerated aging symptoms leading to death at the mean age of 14.6 years usually due to cardiovascular complications. HGPS is caused by a de novo point mutation in the LMNA gene encoding the intermediate filament proteins lamins A and C which are structural components of the nuclear lamina. This mutation leads to the production of a truncated toxic form of lamin A, issued from aberrant splicing and called progerin. Progerin accumulates in HGPS cells' nuclei and is a hallmark of the disease. Small amounts of progerin are also produced during normal aging. HGPS cells and animal preclinical models have provided insights into the molecular and cellular pathways that underlie the disease and have also highlighted possible mechanisms involved in normal aging. This review reports recent medical advances and treatment approaches for patients affected with HGPS.</p>","PeriodicalId":74323,"journal":{"name":"Nucleus (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19491034.2018.1460045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35979442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 71
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