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Cell Adhesion & Migration最新文献

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Expression and molecular insights of lima1 in cholangiocarcinoma. lima1 在胆管癌中的表达和分子研究。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-07-30 DOI: 10.1080/19336918.2024.2383068
Halmurat Obulkasim, Ailiya Adili, Yu Liu, Shaobin Duan
{"title":"Expression and molecular insights of lima1 in cholangiocarcinoma.","authors":"Halmurat Obulkasim, Ailiya Adili, Yu Liu, Shaobin Duan","doi":"10.1080/19336918.2024.2383068","DOIUrl":"10.1080/19336918.2024.2383068","url":null,"abstract":"<p><p>Lim Domain and Actin Binding protein1 (lima1) influence cancer cell function. Thus far, functional role of lima1 in cholangiocarcinoma remains unknown. We used public databases, in vitro experiments, and multi-omics analysis to investigate the Lima1 in cholangiocarcinoma. Our results showed that lima1 expression is significantly upregulated and high levels of lima1 are significantly associated with vascular invasion in cholangiocarcinoma. Furthermore, lima1 knocking out inhibits the RBE cell invasion. Multi-omics data suggest that lima1 affect a broad spectrum of cancer related pathways, promoting tumor progression and metastatic ability in cholangiocarcinoma. This study provides insights into molecular associations of lima1 with tumorigenesist and establishes a preliminary picture of the correlation network in cholangiocarcinoma.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"4-17"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11290767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792051","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
Galectin-1 overexpression induces normal fibroblasts translate into cancer-associated fibroblasts and attenuates the sensitivity of anlotinib in lung cancer. Galectin-1过表达可诱导正常成纤维细胞转化为癌症相关成纤维细胞，并降低肺癌患者对安罗替尼的敏感性。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-04-01 DOI: 10.1080/19336918.2024.2335881
Lei Zhang, Wenbang Chen, Xiaojun Li, Gengming Wang, Fubao Xing, Xiao Zhu
{"title":"Galectin-1 overexpression induces normal fibroblasts translate into cancer-associated fibroblasts and attenuates the sensitivity of anlotinib in lung cancer.","authors":"Lei Zhang, Wenbang Chen, Xiaojun Li, Gengming Wang, Fubao Xing, Xiao Zhu","doi":"10.1080/19336918.2024.2335881","DOIUrl":"10.1080/19336918.2024.2335881","url":null,"abstract":"<p><p>We aimed to investigate galectin-1 overexpression induces normal fibroblasts (NFs) translates into cancer-associated fibroblasts (CAFs). Galectin-1 overexpression was conducted in Human embryonic lung fibroblasts (HFL1) cell. The motilities of H1299 and A549 cells were measured. Human umbilical vein endothelial cell (HUVEC) proliferation and tube formation ability were assessed. Tumor volume and tumor weight was recorded. Cells motilities were increased, while apoptosis rates were decreased after CMs co-cultured. B-cell lymphoma-2 (Bcl-2) expression level was increased, while Bcl2-associatedX (Bax) and cleaved-caspase3 decreased. CMs treatment enhanced HUVEC proliferation and tube formation. Tumor volume and weight in CMs treated mice were increased, and the sensitivity of anlotinib in co-cultured cells was decreased. Our results revealed that galectin-1 overexpression induced NFs translated into CAFs.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10986763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334829","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
Liquid biopsy: paving a new avenue for cancer research. 液体活检：为癌症研究开辟新途径
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-09-01 DOI: 10.1080/19336918.2024.2395807
Keerthi Kurma, Zahra Eslami-S, Catherine Alix-Panabières, Laure Cayrefourcq
{"title":"Liquid biopsy: paving a new avenue for cancer research.","authors":"Keerthi Kurma, Zahra Eslami-S, Catherine Alix-Panabières, Laure Cayrefourcq","doi":"10.1080/19336918.2024.2395807","DOIUrl":"10.1080/19336918.2024.2395807","url":null,"abstract":"<p><p>The current constraints associated with cancer diagnosis and molecular profiling, which rely on invasive tissue biopsies or clinical imaging, have spurred the emergence of the liquid biopsy field. Liquid biopsy involves the extraction of circulating tumor cells (CTCs), circulating free or circulating tumor DNA (cfDNA or ctDNA), circulating cell-free RNA (cfRNA), extracellular vesicles (EVs), and tumor-educated platelets (TEPs) from bodily fluid samples. Subsequently, these components undergo molecular characterization to identify biomarkers that are critical for early cancer detection, prognosis, therapeutic assessment, and post-treatment monitoring. These innovative biosources exhibit characteristics analogous to those of the primary tumor from which they originate or interact. This review comprehensively explores the diverse technologies and methodologies employed for processing these biosources, along with their principal clinical applications.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-26"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11370957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104664","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
Dsg2 ectodomain organization increases throughout desmosome assembly 在整个脱模小体组装过程中，Dsg2 外结构域的组织结构不断增强
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-04-02 DOI: 10.1080/19336918.2024.2333366
William F. Dean, Rose M. Albert, Tomasz J. Nawara, Melanie Ubil, Reena R. Beggs, Alexa L. Mattheyses
{"title":"Dsg2 ectodomain organization increases throughout desmosome assembly","authors":"William F. Dean, Rose M. Albert, Tomasz J. Nawara, Melanie Ubil, Reena R. Beggs, Alexa L. Mattheyses","doi":"10.1080/19336918.2024.2333366","DOIUrl":"https://doi.org/10.1080/19336918.2024.2333366","url":null,"abstract":"Desmosomes are intercellular junctions that regulate mechanical integrity in epithelia and cardiac muscle. Dynamic desmosome remodeling is essential for wound healing and development, yet the mecha...","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"27 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581815","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
A toolbox to analyze collective cell migration, proliferation and cellular organization simultaneously. 同时分析集体细胞迁移、增殖和细胞组织的工具箱。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 Epub Date: 2023-11-08 DOI: 10.1080/19336918.2023.2276615
Urszula Hohmann, Chalid Ghadban, Julian Prell, Christian Strauss, Faramarz Dehghani, Tim Hohmann
{"title":"A toolbox to analyze collective cell migration, proliferation and cellular organization simultaneously.","authors":"Urszula Hohmann, Chalid Ghadban, Julian Prell, Christian Strauss, Faramarz Dehghani, Tim Hohmann","doi":"10.1080/19336918.2023.2276615","DOIUrl":"10.1080/19336918.2023.2276615","url":null,"abstract":"<p><strong>Background: </strong>Analyses of collective cell migration and orientation phenomena are needed to assess the behavior of multicellular clusters. While some tools to the authors' knowledge none is capable to analyze collective migration, cellular orientation and proliferation in phase contrast images simultaneously.</p><p><strong>Methods: </strong>We provide a tool based to analyze phase contrast images of dense cell layers. PIV is used to calculatevelocity fields, while the structure tensor provides cellular orientation. An artificial neural network is used to identify cell division events, allowing to correlate migratory and organizational phenomena with cell density.</p><p><strong>Conclusion: </strong>The presented tool allows the simultaneous analysis of collective cell behavior from phase contrast images in terms of migration, (self-)organization and proliferation.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10773533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71520580","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
Lymphangiogenic responses of lymphatic endothelial cells to steady direct-current electric fields. 淋巴管内皮细胞对稳定直流电场的淋巴管生成反应。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 Epub Date: 2023-10-27 DOI: 10.1080/19336918.2023.2271260
Linbo Guan, Ping Fan, Yufeng Wang, Xinghui Liu, Rui Liu, Wandi Ma, Huai Bai
{"title":"Lymphangiogenic responses of lymphatic endothelial cells to steady direct-current electric fields.","authors":"Linbo Guan, Ping Fan, Yufeng Wang, Xinghui Liu, Rui Liu, Wandi Ma, Huai Bai","doi":"10.1080/19336918.2023.2271260","DOIUrl":"10.1080/19336918.2023.2271260","url":null,"abstract":"<p><p>Lymphangiogenesis plays pivotal roles in diverse physiological and pathological conditions. Steady direct-current electric fields (DC EFs) induce vascular endothelial behaviors related to angiogenesis have been observed. This study investigated the effects of DC EFs on the lymphangiogenic response of lymphatic endothelial cells (LECs). We demonstrated that EFs stimulation induced directional migration, reorientation, and elongation of human LECs in culture. These lymphangiogenic responses required VEGF receptor 3 (VEGFR-3) activation and were mediated through the PI3K-Akt, Erk1/2, and p38 MAPK signaling pathways in relation to the reorganization of the actin cytoskeleton. Our results indicate that endogenous EFs may play a role in lymphangiogenesis in vivo, and VEGFR-3 signaling activation may be involved in the cellular function of LECs driven by EFs.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-14"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54227795","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
MST1/2 in inflammation and immunity. MST1/2在炎症和免疫中的作用。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 Epub Date: 2023-11-01 DOI: 10.1080/19336918.2023.2276616
Tongfen Li, Yiqiong Wen, Qiongfen Lu, Shu Hua, Yunjiao Hou, Xiaohua Du, Yuanyuan Zheng, Shibo Sun
{"title":"MST1/2 in inflammation and immunity.","authors":"Tongfen Li, Yiqiong Wen, Qiongfen Lu, Shu Hua, Yunjiao Hou, Xiaohua Du, Yuanyuan Zheng, Shibo Sun","doi":"10.1080/19336918.2023.2276616","DOIUrl":"10.1080/19336918.2023.2276616","url":null,"abstract":"<p><p>The mammalian Sterile 20-like kinase 1/2 (MST1/2) belongs to the serine/threonine (GC) protein kinase superfamily. Collective studies confirm the vital role MST1/2 in inflammation and immunity. MST1/2 is closely related to the progress of inflammation. Generally, MST1/2 aggravates the inflammatory injury through MST1-JNK, MST1-mROS, MST1-Foxo3, and NF-κB pathways, as well as several regulatory factors such as tumor necrosis factor-α (TNF-α), mitochondrial extension factor 1 (MIEF1), and lipopolysaccharide (LPS). Moreover, MST1/2 is also involved in the regulation of immunity to balance immune activation and tolerance by regulating MST1/2-Rac, MST1-Akt1/c-myc, MST1-Foxos, MST1-STAT, Btk pathways, and lymphocyte function-related antigen 1 (LFA-1), which subsequently prevents immunodeficiency syndrome and autoimmune diseases. This article reviews the effects of MST1/2 on inflammation and immunity.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-15"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71421039","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
A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in β2-integrin activation and signaling. 肉豆蔻酰化富含丙氨酸的C激酶底物（MARCKS）抑制剂肽在β2-整合素激活和信号传导中减弱中性粒细胞。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 DOI: 10.1080/19336918.2023.2233204
Haleigh Conley, Rebecca L Till, Alix K Berglund, Samuel L Jones, M Katie Sheats
{"title":"A myristoylated alanine-rich C-kinase substrate (MARCKS) inhibitor peptide attenuates neutrophil outside-in β<sub>2</sub>-integrin activation and signaling.","authors":"Haleigh Conley, Rebecca L Till, Alix K Berglund, Samuel L Jones, M Katie Sheats","doi":"10.1080/19336918.2023.2233204","DOIUrl":"10.1080/19336918.2023.2233204","url":null,"abstract":"<p><p>MARCKS is an actin and PIP2-binding protein that plays an essential role in neutrophil migration and adhesion; however, the molecular details regarding MARCKS function in these processes remains unclear. Neutrophil adhesion and migration also require the cell surface receptors β<sub>2</sub>-integrins. We hypothesized that MARCKS inhibition would alter neutrophil β<sub>2</sub>-integrin activation and signaling. We utilized a MARCKS-targeting peptide to inhibit MARCKS in inside-out and outside-in β<sub>2</sub>-integrin activation in neutrophils. MANS-mediated MARCKS inhibition had no significant effect on inside-out β<sub>2</sub>-integrin activation. MANS treatment significantly attenuated ICAM-1/Mn<sup>2+</sup>-stimulated static adhesion, cell spreading and β<sub>2</sub>-integrin clustering, suggesting a role for MARCKS function in outside-in β<sub>2</sub>-integrin activation. Additional work is needed to better understand the molecular mechanisms of MARCKS role in outside-in β<sub>2</sub>-integrin activation and signaling.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-16"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fb/1c/KCAM_17_2233204.PMC10348033.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9893102","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
Scribble, Lgl1, and myosin IIA interact with α-/β-catenin to maintain epithelial junction integrity. Scribble, Lgl1和myosin IIA与α-/β-连环蛋白相互作用以维持上皮连接的完整性。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 Epub Date: 2023-09-24 DOI: 10.1080/19336918.2023.2260645
Maha Abedrabbo, Shirel Sloomy, Reham Abu-Leil, Einav Kfir-Cohen, Shoshana Ravid
{"title":"Scribble, Lgl1, and myosin IIA interact with α-/β-catenin to maintain epithelial junction integrity.","authors":"Maha Abedrabbo, Shirel Sloomy, Reham Abu-Leil, Einav Kfir-Cohen, Shoshana Ravid","doi":"10.1080/19336918.2023.2260645","DOIUrl":"10.1080/19336918.2023.2260645","url":null,"abstract":"<p><p>E-cadherin-catenin complex together with the cytoskeleton, builds the core of Adherens junctions (AJs). It has been reported that Scribble stabilizes the coupling of E-cadherin with catenins promoting epithelial cell adhesion, but the mechanism remains unknown. We show that Scribble, Lgl1, and NMII-A reside in a complex with E-cadherin-catenin complex. Depletion of either Scribble or Lgl1 disrupts the localization of E-cadherin-catenin complex to AJs. aPKCζ phosphorylation of Lgl1 regulates AJ localization of Lgl1 and E-cadherin-catenin complexes. Both Scribble and Lgl1 regulate the activation and recruitment of NMII-A at AJs. Finally, Scribble and Lgl1 are downregulated by TGFβ-induced EMT, and their re-expression during EMT impedes its progression. Our results provide insight into the mechanism regulating AJ integrity by Scribble, Lgl1, and NMII-A.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-23"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41178136","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
IL-13 neutralization attenuates carotid artery intimal hyperplasia and increases endothelial cell migration via modulating the JAK-1/STAT-3 signaling pathway. IL-13中和通过调节JAK-1/STAT-3信号通路减轻颈动脉内膜增生并增加内皮细胞迁移。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2023-12-01 Epub Date: 2023-10-09 DOI: 10.1080/19336918.2023.2265158
Qi Li, Yue Li, Fengjiao Wu, Jingyu Li, Zhongsha Li, Xiaoling Qin, Simeng Wei, Chang Chen
{"title":"IL-13 neutralization attenuates carotid artery intimal hyperplasia and increases endothelial cell migration via modulating the JAK-1/STAT-3 signaling pathway.","authors":"Qi Li,&nbsp;Yue Li,&nbsp;Fengjiao Wu,&nbsp;Jingyu Li,&nbsp;Zhongsha Li,&nbsp;Xiaoling Qin,&nbsp;Simeng Wei,&nbsp;Chang Chen","doi":"10.1080/19336918.2023.2265158","DOIUrl":"10.1080/19336918.2023.2265158","url":null,"abstract":"<p><p>The aim of this study was to investigate how the concentration of interleukin-13 (IL-13) affects the regulation of endothelial cell migration after injury. The incubation of recombinant human interleukin-13 (rhIL-13) strongly increased the content of reactive oxygen species (ROS) in HUVECs via the JAK-1/STAT-3/NOX-4 signaling pathway. Antagonizing the high intracellular ROS that was induced by rhIL-13 promoted the migration of HUVECs. Furthermore, IL-13 neutralization not only inhibited intimal hyperplasia, but also promoted the migration of endothelial cells (ECs) after injury. The results suggest that IL-13 inhibition is a potential means of stimulating endothelial cells recovery after injury. Therefore, the attenuation of IL-13 activation may have therapeutic value for vascular disease.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"17 1","pages":"1-10"},"PeriodicalIF":3.2,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/52/f9/KCAM_17_2265158.PMC10566387.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182134","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
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