EMBO ReportsPub Date : 2025-09-22DOI: 10.1038/s44319-025-00585-4
Dan Xiang, Wenfeng Wu, Ruona Shi, Xiaoxiao Tang, Xiaofei Zhang
{"title":"UBE2O-mediated ubiquitylation directs cytoplasmic CTNNA1 to promote cell-to-ECM adhesions.","authors":"Dan Xiang, Wenfeng Wu, Ruona Shi, Xiaoxiao Tang, Xiaofei Zhang","doi":"10.1038/s44319-025-00585-4","DOIUrl":"https://doi.org/10.1038/s44319-025-00585-4","url":null,"abstract":"<p><p>CTNNA1, a multifunctional protein that localizes at both the plasma membrane and the cytosol, plays crucial roles in actin dynamics regulation, cell-to-cell and cell-to-the extracellular matrix (ECM) adhesions and tumor suppression. Despite its diverse functions, the regulatory mechanisms by which cells coordinate CTNNA1's roles remain poorly understood. In this study, we identified UBE2O, a unique hybrid E2/E3 enzyme, as a key regulator that selectively interacts with and ubiquitylates cytosolic CTNNA1 in a phosphorylation-independent manner. Through comprehensive mass spectrometry-based interactome analysis of ubiquitylated CTNNA1, we reveal that the ubiquitylation of CTNNA1 diminishes its interaction with β-catenin while allowing its interaction with vinculin. This switch of molecular interactions promotes focal adhesions maturation, facilitates cell extension and matrix adhesion during the initial phases of cell spreading. Importantly, our findings demonstrate that ubiquitylation serves as a molecular switch that directs the regulatory roles of CTNNA1 to cell-to-ECM adhesions. This study advances our understanding of how ubiquitylation fine-tunes protein function in cell adhesion dynamics.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMBO ReportsPub Date : 2025-09-22DOI: 10.1038/s44319-025-00582-7
Sulayman A Lyons, Micah B S Lea, Mihir Parikh, Zhengzhang Guo, Samrin Kagdi, Abigail R Bisnauth, Jonathan R Pitino, Sabrina Ziai, Negar Mir, Aidan D Tyrrell, Yan Fu, Chuck T Chen, Adam H Metherel, Richard P Bazinet, Bin Yang, Patrick J Knerr, Jonathan D Douros, Jonathan E Campbell, Jacqueline L Beaudry
{"title":"Acute exogenous acyl-GIP treatment enhances lipid handling and fatty acid oxidation by involving brown fat.","authors":"Sulayman A Lyons, Micah B S Lea, Mihir Parikh, Zhengzhang Guo, Samrin Kagdi, Abigail R Bisnauth, Jonathan R Pitino, Sabrina Ziai, Negar Mir, Aidan D Tyrrell, Yan Fu, Chuck T Chen, Adam H Metherel, Richard P Bazinet, Bin Yang, Patrick J Knerr, Jonathan D Douros, Jonathan E Campbell, Jacqueline L Beaudry","doi":"10.1038/s44319-025-00582-7","DOIUrl":"https://doi.org/10.1038/s44319-025-00582-7","url":null,"abstract":"<p><p>The contribution of glucose-dependent insulinotropic polypeptide receptor (GIPR) signalling in brown adipose tissue (BAT) remains underexplored. We studied the acute effects of exogenous acyl-GIP (1 nmol/kg) administration on whole-body lipid handling and fatty acid oxidation, using lipid tolerance tests (LTT) and indirect calorimetry, respectively. We demonstrate that in obese male mice, acute acyl-GIP administration improves lipid tolerance; however, pharmacological inhibition of GIPR, or genetic removal of GIPR globally or with the Myf5-Cre driver, completely abolishes GIP-mediated improvements in lipid tolerance, implicating GIPR in BAT. GIP-mediated improvements in lipid tolerance are associated with an increase in BAT lipid uptake, linked to increases in BAT lipoprotein lipase activity. Our data also reveal that BAT GIPR signalling is necessary for GIP-mediated increases in whole-body fatty acid oxidation, as Myf5-Cre: Gipr mice do not shift substrate oxidation upon GIP administration. Our findings suggest that BAT should be more closely considered in studies examining GIP's effects on whole-body metabolism in rodent models.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Melanocyte differentiation and mechanosensation are differentially modulated by distinct extracellular matrix proteins.","authors":"Carole Luthold, Marie Didion, Vanessa Samira Rácz, Emilio Benedum, Ann-Kathrin Burkhart, Nina Demmerle, Evelyn Wirth, Gubesh Gunaratnam, Sudharshini Thangamurugan, Volkhard Helms, Markus Bischoff, Annika Ridzal, Sandra Iden","doi":"10.1038/s44319-025-00583-6","DOIUrl":"https://doi.org/10.1038/s44319-025-00583-6","url":null,"abstract":"<p><p>Melanocyte dysfunctions can lead to pigmentation disorders or melanoma. Melanocytes interact context-dependently with various types of ECM, including collagens and fibronectin. Alterations in ECM composition and stiffness can impact cell behavior, but their specific roles for melanocyte functions remain unclear. We here exposed melanocytes to different ECM proteins and varying substrate stiffnesses, and identified MITF, a key regulator of melanocyte differentiation and function, as an ECM- and mechanosensitive transcription factor. Moreover, distinct ECM proteins and substrate stiffness engaged a FAK/MEK/ERK/MITF signaling axis to control melanocyte functions. Collagen I restricted FAK and ERK activation, promoting elevated nuclear MITF levels, melanocyte proliferation and a differentiated transcriptomic signature. Conversely, fibronectin elicited FAK and ERK activation, reduced nuclear MITF, increased motility and a dedifferentiated transcriptomic signature. On fibronectin, inhibiting MEK/ERK activity caused increased MITF nuclear localization and enhanced melanogenesis. Additionally, FAK inhibition reduced ERK activation and enhanced melanogenesis, supporting that FAK acts upstream of ERK. Finally, melanocytes show ECM-dependent mechanoresponses. In summary, extrinsic cues exert substantial effects on melanocyte function, involving ERK-dependent MITF regulation.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMBO ReportsPub Date : 2025-09-19DOI: 10.1038/s44319-025-00565-8
Yuto Kegawa, Frances Male, Irene Jiménez-Munguía, Paul S Blank, Elena Mekhedov, Gary E Ward, Joshua Zimmerberg
{"title":"The invasion pore induced by Toxoplasma gondii.","authors":"Yuto Kegawa, Frances Male, Irene Jiménez-Munguía, Paul S Blank, Elena Mekhedov, Gary E Ward, Joshua Zimmerberg","doi":"10.1038/s44319-025-00565-8","DOIUrl":"10.1038/s44319-025-00565-8","url":null,"abstract":"<p><p>The parasite Toxoplasma gondii invades its host cell only after secreting proteins such as invasion-requisite RON2 that inserts into the host cell membrane to establish the moving junction. Electrophysiological recordings at sub-200 µs resolution show a transient increase in host cell membrane conductance following parasite exposure. Transients always precede invasion, but parasites depleted of RON2 generate transients without invading. Thus RON2 is not essential for transient generation. Time-series analysis developed here and applied to the 910,000 data point transient dataset reveal multiple quantal conductance changes in the parasite-induced transient, consistent with rapid insertion, then slower removal, blocking, or inactivation of potential pore components. Quantal steps for wild-type RH strain parasites have a principal mode with Gaussian mean of 0.26 nS, similar in step size to the pore forming protein EXP2, part of the PTEX translocon of malaria parasites. Without RON2 the quantal mean (0.19 nS) is significantly different. Because we observe no parasite invasion without poration, the term \"invasion pore\" is proposed to describe this transient breach in host cell membrane barrier integrity during invasion.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMBO ReportsPub Date : 2025-09-19DOI: 10.1038/s44319-025-00564-9
Frances Male, Yuto Kegawa, Paul S Blank, Irene Jiménez-Munguía, Saima M Sidik, Dylan Valleau, Sebastian Lourido, Maryse Lebrun, Joshua Zimmerberg, Gary E Ward
{"title":"Perforation of the host cell plasma membrane during Toxoplasma invasion requires rhoptry exocytosis.","authors":"Frances Male, Yuto Kegawa, Paul S Blank, Irene Jiménez-Munguía, Saima M Sidik, Dylan Valleau, Sebastian Lourido, Maryse Lebrun, Joshua Zimmerberg, Gary E Ward","doi":"10.1038/s44319-025-00564-9","DOIUrl":"10.1038/s44319-025-00564-9","url":null,"abstract":"<p><p>Toxoplasma gondii is an obligate intracellular parasite. Proteins released during host cell invasion from apical secretory organelles known as rhoptries are delivered into the host cell cytosol to perform functions critical for parasite survival and virulence. How these effector proteins move across the host cell plasma membrane is unknown but may involve a previously noted temporary loss of host cell plasma membrane barrier integrity. Here, we use high-speed, multi-wavelength fluorescence imaging to spatially monitor the barrier integrity of the host cell plasma membrane, in real time, during invasion. The data reveal that early in invasion the parasite creates a transient perforation in the host cell membrane. The perforation occurs at the point on the host membrane in contact with the parasite's apical end. Parasites depleted of any of five proteins known to be required for rhoptry exocytosis are unable to perforate the host cell membrane. These data suggest a model in which perforating agents stored within rhoptries are released onto the host cell at the initiation of invasion to create a conduit for the delivery of rhoptry effector proteins.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMBO ReportsPub Date : 2025-09-16DOI: 10.1038/s44319-025-00578-3
Sushil Kumar, Xuan Ji, Hina Iqbal, Xiangnan Guan, Brittany Mis, Devanshi Dave, Suresh Kumar, Jacob Besler, Ranjan Dash, Zheng Xia, Ravi K Singh
{"title":"The muscle specific MEF2Dα2 isoform promotes muscle ketolysis and running capacity in mice.","authors":"Sushil Kumar, Xuan Ji, Hina Iqbal, Xiangnan Guan, Brittany Mis, Devanshi Dave, Suresh Kumar, Jacob Besler, Ranjan Dash, Zheng Xia, Ravi K Singh","doi":"10.1038/s44319-025-00578-3","DOIUrl":"https://doi.org/10.1038/s44319-025-00578-3","url":null,"abstract":"<p><p>During prolonged starvation and exhaustive exercise, when there is low availability of carbohydrates, the liver breaks down fatty acids to generate ketone bodies, which are utilized by peripheral tissues as an alternative fuel source. The transcription factor MEF2D undergoes regulated alternative splicing in the postnatal period to produce a highly conserved, muscle specific MEF2Dα2 protein isoform. Here, we discover that compared to WT mice, MEF2Dα2 exon knockout (Eko) mice display reduced running capacity and muscle expression of all three ketolytic enzymes: BDH1, OXCT1, and ACAT1. MEF2Dα2 Eko mice consistently show increased blood ketone body levels in a tolerance test, after exercise, and when fed a ketogenic diet. Lastly, using mitochondria isolated from skeletal muscle, Eko mice show reduced ketone body utilization compared to WT mice. Collectively, our findings identify a new role for the MEF2Dα2 protein isoform in regulating skeletal muscle ketone body oxidation, exercise capacity, and systemic ketone body levels.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Phosphatase PTPN22 functions as an adaptor in the mTORC2 complex.","authors":"Keshav Gupta, Nagalakshmi Kommineni, Tanuja Bogadi, Neeraja P Alamuru-Yellapragada, Subbareddy Maddika","doi":"10.1038/s44319-025-00576-5","DOIUrl":"https://doi.org/10.1038/s44319-025-00576-5","url":null,"abstract":"<p><p>mTOR (mechanistic target of rapamycin) kinase is a pivotal regulator of cellular growth and metabolism, integrating signals from nutrients and growth factors. It functions through the assembly of two distinct complexes, mTORC1 and mTORC2, which differ in their substrate specificity and regulation. While the regulation of mTORC1 is well-characterized, less is known about the modulators of mTORC2 signaling. In this study, we identify tyrosine phosphatase PTPN22 as an mTORC2-associated protein. We provide evidence that PTPN22 is essential for the activation of the mTORC2/AKT axis, independent of cell lineage. Loss of PTPN22 results in impaired AKT phosphorylation in response to both basal and growth factor signals. Mechanistically, PTPN22 functions as a scaffolding protein that promotes the mSIN-RICTOR interaction, thereby maintaining mTORC2 complex integrity. Notably, this adaptor function of PTPN22 is independent of its tyrosine phosphatase activity. Functionally, we demonstrate that PTPN22 is required for cell growth and survival in both cellular models and nude mouse xenografts. Together, these findings reveal a non-catalytic role for phosphatase PTPN22 in mTORC2 assembly and function.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CDC42 supports HBV entry by NTCP translocation to the plasma membrane and macropinocytosis.","authors":"Shuzhi Cui, Wei Gao, Yuxin Chen, Yi Xu, Zhifang Li, Yu Wei, Yaming Jiu","doi":"10.1038/s44319-025-00581-8","DOIUrl":"https://doi.org/10.1038/s44319-025-00581-8","url":null,"abstract":"<p><p>CDC42 is a member of Rho GTPase family that regulates various biological processes and its activity can be hijacked by invading pathogens. Here, we discovered that the level of active CDC42 in hepatocytes positively correlates with the entry capacity of hepatitis B virus (HBV). Mechanistically, CDC42 activation effectively promotes the transport of the viral receptor sodium taurocholate co-transporting polypeptide (NTCP) to the plasma membrane via Rab11 dependent recycling endosomal pathway. NTCP interacts with Rab11 and activation of CDC42 signaling reinforces the interaction between NTCP and Rab11. We further show that clathrin mediated endocytosis (CME), the known HBV entry pathway, is independent of CDC42 activity. Intriguingly, we reveal that CDC42 dependent macropinocytosis is a route for HBV entry, which is equally essential for viral infection as CME. Together, our findings uncover new mechanisms for HBV entry that involve unrecognized functions of CDC42 and suggest that Rho GTPase signaling might represent a potential target for antiviral therapy.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMBO ReportsPub Date : 2025-09-15DOI: 10.1038/s44319-025-00580-9
Riikka Pietilä, Guillem Genové, Giuseppe Mocci, Yuyang Miao, Jianping Liu, Stefanos Leptidis, Francesca Del Gaudio, Martin Uhrbom, Elisa Vázquez-Liébanas, Sonja Gustafsson, Byambajav Buyandelger, Elisabeth Raschperger, Johan L M Björkegren, Emil M Hansson, Konstantin Gaengel, Maarja Andaloussi Mäe, Marie Jeansson, Michael Vanlandewijck, Liqun He, Carina Strell, Xiao-Rong Peng, Urban Lendahl, Christer Betsholtz, Lars Muhl
{"title":"A comprehensive molecular atlas of the mesenchymal cell types in the mouse liver.","authors":"Riikka Pietilä, Guillem Genové, Giuseppe Mocci, Yuyang Miao, Jianping Liu, Stefanos Leptidis, Francesca Del Gaudio, Martin Uhrbom, Elisa Vázquez-Liébanas, Sonja Gustafsson, Byambajav Buyandelger, Elisabeth Raschperger, Johan L M Björkegren, Emil M Hansson, Konstantin Gaengel, Maarja Andaloussi Mäe, Marie Jeansson, Michael Vanlandewijck, Liqun He, Carina Strell, Xiao-Rong Peng, Urban Lendahl, Christer Betsholtz, Lars Muhl","doi":"10.1038/s44319-025-00580-9","DOIUrl":"https://doi.org/10.1038/s44319-025-00580-9","url":null,"abstract":"<p><p>The liver plays crucial roles in many essential physiological processes, and its impaired function due to liver fibrosis from various causes is an increasingly significant health issue. The liver's functionality relies on the precise arrangement of its cellular structures, yet the molecular architecture of these units remains only partially understood. We created a comprehensive molecular atlas detailing the major cell types present in the adult mouse liver through deep single-cell RNA sequencing. Our analysis offers new insights into hepatic endothelial and mesenchymal cells, specifically highlighting the diversity of cells in the periportal microvasculature, the sinusoids, and the portal vein, the latter exhibiting a mixed arterio-venous phenotype. We identified distinct subpopulations of hepatic stellate cells, fibroblasts, and vascular mural cells located in different anatomical liver regions. Comparisons with transcriptomic data from disease models indicate that a previously unrecognized capsular population of hepatic stellate cells expands in response to fibrotic disease. Our findings reveal that various fibroblast subpopulations respond differently to pathological insults. This data resource will be relevant for the advancement of therapies targeting hepatic diseases.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CDK1-mediated phosphorylation of LDHA fuels mitosis through LDHB-dependent lactate oxidation.","authors":"Mengting Liu, Aoxing Cheng, Weiyi You, Jiaxin Wu, Chenxu Dai, Ting Wang, Ying Wu, Fumei Zhong, Jue Shi, Yingying Du, Zhonghuai Hou, Ping Gao, Ke Ruan, Yi Yang, Yuzheng Zhao, Kaiguang Zhang, Zhenye Yang, Jing Guo","doi":"10.1038/s44319-025-00573-8","DOIUrl":"https://doi.org/10.1038/s44319-025-00573-8","url":null,"abstract":"<p><p>While cancer cells overexpress lactate dehydrogenase A (LDHA) to support glycolytic flux and lactate production, the role of LDHB-which preferentially catalyzes lactate oxidation-remains unclear. Here, we demonstrate that LDHB, but not LDHA, is essential for mitotic progression in cancers. During mitosis, CDK1 phosphorylates LDHA at threonine 18, reducing its incorporation into the lactate dehydrogenase (LDH) tetramer. This results in LDHB-enriched tetramers that shift catalytic activity toward lactate oxidation, converting lactate and NAD⁺ into pyruvate and NADH. The generated NADH fuels oxidative phosphorylation and ATP production, thereby sustaining mitosis. Notably, LDHA-T18 phosphorylation occurs exclusively in tumor tissues. Our findings reveal a tumor-specific mechanism in which CDK1 reprograms LDH isoenzyme composition to direct lactate toward NADH production, ensuring energy homeostasis during mitosis. This underscores the therapeutic necessity of targeting both LDHA and LDHB in cancer.</p>","PeriodicalId":11541,"journal":{"name":"EMBO Reports","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}