Journal of Cell Biology最新文献_第2页

Submembrane liprin-α1 clusters spatially localize insulin granule fusion. 膜下脂素-α1簇在空间上定位胰岛素颗粒融合。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-08-28 DOI: 10.1083/jcb.202410210

Kylie Deng, Kitty Sun, Nicole Hallahan, Wan Jun Gan, Michelle Cielesh, Baharak Mahyad, Melkam A Kebede, Mark Larance, Peter Thorn

{"title":"Submembrane liprin-α1 clusters spatially localize insulin granule fusion.","authors":"Kylie Deng, Kitty Sun, Nicole Hallahan, Wan Jun Gan, Michelle Cielesh, Baharak Mahyad, Melkam A Kebede, Mark Larance, Peter Thorn","doi":"10.1083/jcb.202410210","DOIUrl":"https://doi.org/10.1083/jcb.202410210","url":null,"abstract":"Insulin granule fusion in pancreatic β cells localizes to where they contact the ECM of the islet capillaries. The mechanism(s) underpinning localization are unclear. Using glucose or high K+ stimulation or the global uncaging of Ca2+, we show granule fusion consistently focused to the β cell-ECM interface, suggesting a specific localization mechanism. We tested for the involvement of liprin-α1, a scaffold protein enriched at the β cell-ECM interface. Liprin-α1 knockdown did not affect high K+-stimulated insulin secretion but did impair localization of exocytosis. Liprin-α1 knockdown impaired glucose-induced insulin secretion with evidence that the C-terminal of liprin-α1 positions liprin-α1 in clusters at the β cell-ECM interface. Liprin-α1 cluster size and number are regulated by glucose, and exocytosis is spatially coupled with the clusters. Immunoprecipitation and mass spectrometry characterized a liprin-α1 interactome, including β2-syntrophin, an insulin granule-linked protein. We conclude that liprin-α1 is part of a complex that is regulated by glucose and locally targets insulin granules to the β cell-ECM interface.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12393827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ATG conjugation-dependent/independent mechanisms underlie lysosomal stress-induced TFEB regulation. ATG偶联依赖/独立机制是溶酶体应激诱导TFEB调控的基础。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-08-29 DOI: 10.1083/jcb.202307079

Shiori Akayama, Takayuki Shima, Tatsuya Kaminishi, Mengying Cui, Jlenia Monfregola, Kohei Nishino, Andrea Ballabio, Hidetaka Kosako, Tamotsu Yoshimori, Shuhei Nakamura

{"title":"ATG conjugation-dependent/independent mechanisms underlie lysosomal stress-induced TFEB regulation.","authors":"Shiori Akayama, Takayuki Shima, Tatsuya Kaminishi, Mengying Cui, Jlenia Monfregola, Kohei Nishino, Andrea Ballabio, Hidetaka Kosako, Tamotsu Yoshimori, Shuhei Nakamura","doi":"10.1083/jcb.202307079","DOIUrl":"https://doi.org/10.1083/jcb.202307079","url":null,"abstract":"TFEB, a master regulator of autophagy and lysosomal biogenesis, is activated by several cellular stresses including lysosomal damage, but its underlying mechanism is unclear. TFEB activation during lysosomal damage depends on the ATG conjugation system, which mediates lipidation of ATG8 proteins. Here, we newly identify ATG conjugation-independent TFEB regulation that precedes ATG conjugation-dependent regulation, designated Modes I and II, respectively. We reveal unique regulators of TFEB in each mode: APEX1 in Mode I and CCT7 and/or TRIP6 in Mode II. APEX1 interacts with TFEB independently of the ATG conjugation system, and is required for TFEB stability, while both CCT7 and TRIP6 accumulate on lysosomes during lysosomal damage, and interact with TFEB mainly in ATG conjugation system-deficient cells, presumably blocking TFEB activation. TFEB activation by several other stresses also involves either Mode I or Mode II. Our results pave the way for a unified understanding of TFEB regulatory mechanisms from the perspective of the ATG conjugation system under a variety of cellular stresses.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12396377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Multiple golgins are required to support extracellular matrix secretion, modification, and assembly. 需要多个高尔金来支持细胞外基质的分泌、修饰和组装。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-08-18 DOI: 10.1083/jcb.202411167

George Thompson, Anna Hoyle, Philip A Lewis, M Esther Prada-Sanchez, Joe Swift, Kate Heesom, Martin Lowe, David Stephens, Nicola L Stevenson

{"title":"Multiple golgins are required to support extracellular matrix secretion, modification, and assembly.","authors":"George Thompson, Anna Hoyle, Philip A Lewis, M Esther Prada-Sanchez, Joe Swift, Kate Heesom, Martin Lowe, David Stephens, Nicola L Stevenson","doi":"10.1083/jcb.202411167","DOIUrl":"10.1083/jcb.202411167","url":null,"abstract":"The secretion of extracellular matrix (ECM) proteins is vital to the maintenance of tissue health. One major control point of this process is the Golgi apparatus, whose dysfunction causes numerous connective tissue disorders. We therefore sought to investigate the role of two Golgi organizing proteins, GMAP210 and Golgin-160, in ECM secretion. CRISPR knockout of either protein had distinct impacts on Golgi organization, with Golgin-160 knockout causing Golgi fragmentation and vesicle accumulation, and GMAP210 loss leading to cisternal fragmentation, dilation, and the accumulation of tubulovesicular structures. Both golgins were required for fibrillar collagen organization and glycosaminoglycan synthesis suggesting nonredundant functions in these processes. Furthermore, proteomics analysis revealed both shared and golgin-specific changes in the secretion of ECM proteins. We therefore propose that golgins are collectively required to create the correct physical-chemical space to support efficient ECM protein secretion, modification, and assembly. This is the first time that Golgin-160 has been shown to be required for ECM secretion.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Multi-kinesin clusters impart mechanical stress that reveals mechanisms of microtubule breakage in cells. 多动力蛋白簇传递机械应力，揭示细胞微管断裂的机制。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-08-11 DOI: 10.1083/jcb.202501070

Qi Geng, Andres Bonilla, Siara N Sandwith, Kristen J Verhey

{"title":"Multi-kinesin clusters impart mechanical stress that reveals mechanisms of microtubule breakage in cells.","authors":"Qi Geng, Andres Bonilla, Siara N Sandwith, Kristen J Verhey","doi":"10.1083/jcb.202501070","DOIUrl":"10.1083/jcb.202501070","url":null,"abstract":"Microtubules are cytoskeletal filaments that provide structural support for numerous cellular processes. Despite their high rigidity, microtubules can be dramatically bent in cells, and it is unknown how much force a microtubule can withstand before breaking. We find that the kinesin-3 motor KIF1C forms condensates that entangle and break neighboring microtubules. Combining computational simulations and experiments, we show that microtubule breakage is an emergent property that is dependent on a highly processive kinesin motor domain, the cluster properties, cytoplasmic viscosity, and microtubule anchors. We estimate a rupture force for microtubules in cells that is lower than previous estimates based on in vitro studies with taxol-stabilized microtubules. The absence of microtubule breakage under physiological conditions suggests that mechanisms exist to protect microtubule integrity, which may inform about physical constraints on the evolution of motor proteins. We suggest that release of either the motor-cargo or motor-microtubule interaction prevents the accumulation of mechanical stress upon the engagement of multi-motor clusters with microtubules.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816747","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}

引用次数: 0

AI-directed voxel extraction and volume EM identify intrusions as sites of mitochondrial contact. 人工智能引导的体素提取和体积EM将入侵识别为线粒体接触点。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-07-30 DOI: 10.1083/jcb.202411138

Benjamin S Padman, Runa S J Lindblom, Michael Lazarou

{"title":"AI-directed voxel extraction and volume EM identify intrusions as sites of mitochondrial contact.","authors":"Benjamin S Padman, Runa S J Lindblom, Michael Lazarou","doi":"10.1083/jcb.202411138","DOIUrl":"10.1083/jcb.202411138","url":null,"abstract":"Membrane contact sites (MCSs) establish organelle interactomes in cells to enable communication and exchange of materials. Volume EM (vEM) is ideally suited for MCS analyses, but semantic segmentation of large vEM datasets remains challenging. Recent adoption of artificial intelligence (AI) for segmentation has greatly enhanced our analysis capabilities. However, we show that organelle boundaries, which are important for defining MCS, are the least confident predictions made by AI. We outline a segmentation strategy termed AI-directed voxel extraction (AIVE), which refines segmentation results and boundary predictions derived from any AI-based method by combining those results with electron signal values. We demonstrate the precision conferred by AIVE by applying it to the quantitative analysis of organelle interactomes from multiple FIB-SEM datasets. Through AIVE, we discover a previously unknown category of mitochondrial contact that we term the mitochondrial intrusion. We hypothesize that intrusions serve as anchors that stabilize MCS and promote organelle communication.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Telomeric SUMO level influences the choices of APB formation pathways and ALT efficiency. 端粒SUMO水平影响APB形成途径的选择和ALT效率。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-09-03 DOI: 10.1083/jcb.202410073

Rongwei Zhao, Xiaoyang Yu, Tafadzwa Chigumira, Meng Xu, Allison Wivagg, Rachel M Lackner, Jayme Salsman, Graham Dellaire, Michael J Matunis, David M Chenoweth, Xiaolan Zhao, Huaiying Zhang

{"title":"Telomeric SUMO level influences the choices of APB formation pathways and ALT efficiency.","authors":"Rongwei Zhao, Xiaoyang Yu, Tafadzwa Chigumira, Meng Xu, Allison Wivagg, Rachel M Lackner, Jayme Salsman, Graham Dellaire, Michael J Matunis, David M Chenoweth, Xiaolan Zhao, Huaiying Zhang","doi":"10.1083/jcb.202410073","DOIUrl":"10.1083/jcb.202410073","url":null,"abstract":"Many cancers use an alternative lengthening of telomeres (ALT) pathway for telomere maintenance. ALT telomeric DNA synthesis occurs in ALT-associated PML bodies (APBs). However, the mechanisms by which APBs form are not well understood. Here, we monitored the formation of APBs with time-lapse imaging employing CRISPR knock-in to track the promyelocytic leukemia (PML) protein at endogenous levels. We found APBs form via two pathways: telomeres recruit PML proteins to nucleate PML bodies de novo, or telomeres fuse with preformed PML bodies. Both nucleation and fusion of APBs require interactions between SUMO and SUMO interaction motifs (SIMs). Moreover, APB nucleation is associated with higher levels of SUMO and SUMO-mediated recruitment of DNA helicase BLM, resulting in more robust telomeric DNA synthesis. Finally, further boosting SUMO levels at telomeres enhances APB nucleation, BLM enrichment, and telomeric DNA synthesis. Thus, high SUMO levels at telomeres promote APB nucleation and stronger ALT activity.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Mitochondrial fission controls astrocyte morphogenesis and organization in the cortex. 线粒体分裂控制皮层星形胶质细胞的形态发生和组织。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-09-03 DOI: 10.1083/jcb.202410130

Maria Pia Rodriguez Salazar, Sprihaa Kolanukuduru, Valentina Ramirez, Boyu Lyu, Gracie Manigault, Gabrielle Sejourne, Hiromi Sesaki, Guoqiang Yu, Cagla Eroglu

{"title":"Mitochondrial fission controls astrocyte morphogenesis and organization in the cortex.","authors":"Maria Pia Rodriguez Salazar, Sprihaa Kolanukuduru, Valentina Ramirez, Boyu Lyu, Gracie Manigault, Gabrielle Sejourne, Hiromi Sesaki, Guoqiang Yu, Cagla Eroglu","doi":"10.1083/jcb.202410130","DOIUrl":"10.1083/jcb.202410130","url":null,"abstract":"Dysfunctional mitochondrial dynamics are a hallmark of devastating neurodevelopmental disorders such as childhood refractory epilepsy. However, the role of glial mitochondria in proper brain development is not well understood. We show that astrocyte mitochondria undergo extensive fission while populating astrocyte distal branches during postnatal cortical development. Loss of mitochondrial fission regulator, dynamin-related protein 1 (Drp1), decreases mitochondrial localization to distal astrocyte processes, and this mitochondrial mislocalization reduces astrocyte morphological complexity. Functionally, astrocyte-specific conditional deletion of Drp1 induces astrocyte reactivity and disrupts astrocyte organization in the cortex. These morphological and organizational deficits are accompanied by loss of perisynaptic astrocyte process (PAP) proteins such as gap junction protein connexin 43. These findings uncover a crucial role for mitochondrial fission in coordinating astrocytic morphogenesis and organization, revealing the regulation of astrocytic mitochondrial dynamics as a critical step in neurodevelopment.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Kinesin-8/Kip3 requires beta tubulin tail for depolymerase activity. 激酶8/Kip3需要β微管蛋白尾部来维持解聚合酶的活性。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-09-08 DOI: 10.1083/jcb.202501219

Kaitlin Alemany, Samantha Johnson, Jeffrey K Moore

引用次数: 0

Stu2 performs an essential kinetochore function independent of its microtubule polymerase activity. Stu2执行独立于微管聚合酶活性的基本着丝点功能。

IF 6.4 1区生物学

Journal of Cell Biology Pub Date : 2025-10-06 Epub Date: 2025-09-03 DOI: 10.1083/jcb.202209025

Ahmed A Abouelghar, Joseph S Carrier, Julia R Torvi, Erin Jenson, Chloe Jones, Binnu Gangadharan, Elisabeth G Prinslow, Luke M Rice, Brent Lagesse, Georjana Barnes, Matthew P Miller

{"title":"Stu2 performs an essential kinetochore function independent of its microtubule polymerase activity.","authors":"Ahmed A Abouelghar, Joseph S Carrier, Julia R Torvi, Erin Jenson, Chloe Jones, Binnu Gangadharan, Elisabeth G Prinslow, Luke M Rice, Brent Lagesse, Georjana Barnes, Matthew P Miller","doi":"10.1083/jcb.202209025","DOIUrl":"10.1083/jcb.202209025","url":null,"abstract":"ch-TOG family proteins, including the budding yeast Stu2, are essential for spindle formation and chromosome segregation. Such functions depend on an array of activities ranging from microtubule nucleation, polymerization, and depolymerization to conferring tension sensitivity to kinetochores. This functional diversity makes it challenging to dissect these various functions and understand their relative importance. Here, we developed separation-of-function mutants and used artificial tethering tools to elucidate several important mechanistic insights into Stu2's essential role. We show that Stu2's microtubule polymerization activity depends on its basic linker region but is surprisingly dispensable for viability; that in fact, Stu2 carries out an essential kinetochore-associated function; and finally, that Stu2's precise location within the kinetochore is critical for its function, suggesting a spatial separation mode of action may underlie its ability to confer tension sensitivity. Our findings highlight the significance of Stu2's kinetochore role and provide insights into the molecular mechanisms by which it performs its various functions.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"224 10","pages":""},"PeriodicalIF":6.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

SCFFBXO21-mediated ubiquitination and degradation of NMNAT2 regulates axon survival in nerve injury. scffbxo21介导的泛素化和NMNAT2降解调节神经损伤中的轴突存活。

IF 7.8 1区生物学

Journal of Cell Biology Pub Date : 2025-09-30 DOI: 10.1083/jcb.202501072

Wenjing Long,Shunyi Li,Qiangqiang Wang,Wenkai Yue,Yanbin Fu,Haiqiong Wang,Mingsheng Jiang,Xianyan Hu,Yunxia Li,Jihong Cui,Ang Li,Yaoyang Zhang,Zairong Zhang,Yanshan Fang

{"title":"SCFFBXO21-mediated ubiquitination and degradation of NMNAT2 regulates axon survival in nerve injury.","authors":"Wenjing Long,Shunyi Li,Qiangqiang Wang,Wenkai Yue,Yanbin Fu,Haiqiong Wang,Mingsheng Jiang,Xianyan Hu,Yunxia Li,Jihong Cui,Ang Li,Yaoyang Zhang,Zairong Zhang,Yanshan Fang","doi":"10.1083/jcb.202501072","DOIUrl":"https://doi.org/10.1083/jcb.202501072","url":null,"abstract":"NMNAT2 is an essential but labile protein required for axon integrity. It is rapidly degraded after nerve injury, promoting axon degeneration. However, the mechanisms regulating NMNAT2 ubiquitination and turnover in neurons remain unclear. In this study, we identify the F-box protein FBXO21 as an NMNAT2-binding protein, and its deficiency confers axonal protection via increasing NMNAT2 abundance. FBXO21 recruits SKP1, CUL1, and RBX1 to form an SCFFBXO21 complex, which promotes NMNAT2 ubiquitination in vivo and in vitro. SCFFBXO21 ubiquitinates NMNAT2 at K155 within an isoform-specific targeting and interaction domain of the family of NMNATs, which underlies the unique labile nature of NMNAT2. The ubiquitination-deficient NMNAT2-K155R exhibits substantially reduced protein turnover and enhanced axon-protective capacity. Finally, in Fbxo21 knockout mice, NMNAT2 levels are markedly increased and the survival of injured sciatic nerves is significantly prolonged. Collectively, our findings reveal a crucial role of FBXO21 in axon degeneration, highlighting the SCFFBXO21 complex as a potential target for modulating NMNAT2-dependent axon survival.","PeriodicalId":15211,"journal":{"name":"Journal of Cell Biology","volume":"24 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194783","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}

引用次数: 0