The Journal of Cell Biology最新文献_第10页

In situ cryo-electron tomography reveals local cellular machineries for axon branch development 原位冷冻电子断层扫描揭示了轴突分支发育的局部细胞机制

The Journal of Cell Biology Pub Date : 2021-07-29 DOI: 10.1083/jcb.202106086

Hana Nedozrálová, Nirakar Basnet, Iosune Ibiricu, Satish Bodakuntla, Christian Biertümpfel, N. Mizuno

{"title":"In situ cryo-electron tomography reveals local cellular machineries for axon branch development","authors":"Hana Nedozrálová, Nirakar Basnet, Iosune Ibiricu, Satish Bodakuntla, Christian Biertümpfel, N. Mizuno","doi":"10.1083/jcb.202106086","DOIUrl":"https://doi.org/10.1083/jcb.202106086","url":null,"abstract":"Neurons are highly polarized cells forming an intricate network of dendrites and axons. They are shaped by the dynamic reorganization of cytoskeleton components and cellular organelles. Axon branching allows to form new paths and increases circuit complexity. However, our understanding of branch formation is sparse due to technical limitations. Using in situ cellular cryo-electron tomography on primary mouse neurons, we directly visualized the remodeling of organelles and cytoskeleton structures at axon branches. Strikingly, branched areas functioned as hotspots concentrating organelles to support dynamic activities. Unaligned actin filaments assembled at the base of premature branches and remained while filopodia diminished. Microtubules and ER co-migrated into preformed branches to support outgrowth together with accumulating compact ~500 nm mitochondria and locally clustered ribosomes. We obtained a roadmap of events and present the first direct evidence of local protein synthesis selectively taking place at axon branches, allowing to serve as unique control hubs for axon development and downstream neural network formation.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134283797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Tensin3 interaction with talin drives the formation of fibronectin-associated fibrillar adhesions Tensin3与talin相互作用驱动纤维连接蛋白相关纤维粘连的形成

The Journal of Cell Biology Pub Date : 2021-07-16 DOI: 10.1101/2021.07.16.452612

P. Atherton, Rafaella Konstantinou, S. P. Neo, Emily Wang, Eleonora Balloi, M. Ptushkina, Hayley Bennett, K. Clark, J. Gunaratne, D. Critchley, I. Barsukov, E. Manser, C. Ballestrem

{"title":"Tensin3 interaction with talin drives the formation of fibronectin-associated fibrillar adhesions","authors":"P. Atherton, Rafaella Konstantinou, S. P. Neo, Emily Wang, Eleonora Balloi, M. Ptushkina, Hayley Bennett, K. Clark, J. Gunaratne, D. Critchley, I. Barsukov, E. Manser, C. Ballestrem","doi":"10.1101/2021.07.16.452612","DOIUrl":"https://doi.org/10.1101/2021.07.16.452612","url":null,"abstract":"The formation of healthy tissue involves continuous remodelling of the extracellular matrix (ECM). Whilst it is known that this requires integrin-associated cell-ECM adhesion sites (CMAs) and actomyosin-mediated forces, the underlying mechanisms remain unclear. Here we examine how tensin3 contributes to formation of fibrillar adhesions (FBs) and fibronectin fibrillo-genesis. Using BioID mass spectrometry and a mitochondrial targeting assay, we establish that tensin3 associates with the mechanosensors talin and vinculin. We show that the talin R11 rod domain binds directly to a helical motif within the central intrinsically disordered region (IDR) of tensin3, whilst vinculin binds indirectly to tensin3 via talin. Using CRISPR knock-out cells in combination with defined tensin3 mutations, we show (i) that tensin3 is critical for formation of α5β1-integrin FBs and for fibronectin fibrillogenesis, and (ii) the talin/tensin3 interaction drives this process, with vinculin acting to potentiate it.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126488695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Per1/Per2-Igf2 axis-mediated circadian regulation of myogenic differentiation. Per1/Per2-Igf2轴介导的肌源性分化昼夜节律调节。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-19 DOI: 10.1083/jcb.202101057

Nobuko Katoku-Kikyo, Ellen Paatela, Daniel L Houtz, Britney Lee, Dane Munson, Xuerui Wang, Mohammed Hussein, Jasmeet Bhatia, Seunghyun Lim, Ce Yuan, Yoko Asakura, Atsushi Asakura, Nobuaki Kikyo

{"title":"Per1/Per2-Igf2 axis-mediated circadian regulation of myogenic differentiation.","authors":"Nobuko Katoku-Kikyo, Ellen Paatela, Daniel L Houtz, Britney Lee, Dane Munson, Xuerui Wang, Mohammed Hussein, Jasmeet Bhatia, Seunghyun Lim, Ce Yuan, Yoko Asakura, Atsushi Asakura, Nobuaki Kikyo","doi":"10.1083/jcb.202101057","DOIUrl":"https://doi.org/10.1083/jcb.202101057","url":null,"abstract":"Circadian rhythms regulate cell proliferation and differentiation, but circadian control of tissue regeneration remains elusive at the molecular level. Here, we show that proper myoblast differentiation and muscle regeneration are regulated by the circadian master regulators Per1 and Per2. Depletion of Per1 or Per2 suppressed myoblast differentiation in vitro and muscle regeneration in vivo, demonstrating their nonredundant functions. Both Per1 and Per2 were required for the activation of Igf2, an autocrine promoter of myoblast differentiation, accompanied by Per-dependent recruitment of RNA polymerase II, dynamic histone modifications at the Igf2 promoter and enhancer, and the promoter-enhancer interaction. This circadian epigenetic priming created a preferred time window for initiating myoblast differentiation. Consistently, muscle regeneration was faster if initiated at night, when Per1, Per2, and Igf2 were highly expressed compared with morning. This study reveals the circadian timing as a significant factor for effective muscle cell differentiation and regeneration.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/df/0b/JCB_202101057.PMC8138781.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39009871","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: 10

Selective MAP1LC3C (LC3C) autophagy requires noncanonical regulators and the C-terminal peptide. 选择性MAP1LC3C (LC3C)自噬需要非规范调节因子和c端肽。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-14 DOI: 10.1083/jcb.202004182

Megan E Bischoff, Yuanwei Zang, Johnson Chu, Adam D Price, Birgit Ehmer, Nicholas J Talbot, Michael J Newbold, Anurag Paul, Jun-Lin Guan, David R Plas, Jarek Meller, Maria F Czyzyk-Krzeska

{"title":"Selective MAP1LC3C (LC3C) autophagy requires noncanonical regulators and the C-terminal peptide.","authors":"Megan E Bischoff, Yuanwei Zang, Johnson Chu, Adam D Price, Birgit Ehmer, Nicholas J Talbot, Michael J Newbold, Anurag Paul, Jun-Lin Guan, David R Plas, Jarek Meller, Maria F Czyzyk-Krzeska","doi":"10.1083/jcb.202004182","DOIUrl":"https://doi.org/10.1083/jcb.202004182","url":null,"abstract":"LC3s are canonical proteins necessary for the formation of autophagosomes. We have previously established that two paralogs, LC3B and LC3C, have opposite activities in renal cancer, with LC3B playing an oncogenic role and LC3C a tumor-suppressing role. LC3C is an evolutionary late gene present only in higher primates and humans. Its most distinct feature is a C-terminal 20-amino acid peptide cleaved in the process of glycine 126 lipidation. Here, we investigated mechanisms of LC3C-selective autophagy. LC3C autophagy requires noncanonical upstream regulatory complexes that include ULK3, UVRAG, RUBCN, PIK3C2A, and a member of ESCRT, TSG101. We established that postdivision midbody rings (PDMBs) implicated in cancer stem-cell regulation are direct targets of LC3C autophagy. LC3C C-terminal peptide is necessary and sufficient to mediate LC3C-dependent selective degradation of PDMBs. This work establishes a new noncanonical human-specific selective autophagic program relevant to cancer stem cells.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e8/a5/JCB_202004182.PMC8129795.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38912185","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: 6

Mechanism of mutant calreticulin-mediated activation of the thrombopoietin receptor in cancers. 突变钙调蛋白介导的癌症血小板生成素受体激活机制。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 DOI: 10.1083/jcb.202009179

Arunkumar Venkatesan, Jie Geng, Malathi Kandarpa, Sanjeeva Joseph Wijeyesakere, Ashwini Bhide, Moshe Talpaz, Irina D Pogozheva, Malini Raghavan

{"title":"Mechanism of mutant calreticulin-mediated activation of the thrombopoietin receptor in cancers.","authors":"Arunkumar Venkatesan, Jie Geng, Malathi Kandarpa, Sanjeeva Joseph Wijeyesakere, Ashwini Bhide, Moshe Talpaz, Irina D Pogozheva, Malini Raghavan","doi":"10.1083/jcb.202009179","DOIUrl":"https://doi.org/10.1083/jcb.202009179","url":null,"abstract":"Myeloproliferative neoplasms (MPNs) are frequently driven by mutations within the C-terminal domain (C-domain) of calreticulin (CRT). CRTDel52 and CRTIns5 are recurrent mutations. Oncogenic transformation requires both mutated CRT and the thrombopoietin receptor (Mpl), but the molecular mechanism of CRT-mediated constitutive activation of Mpl is unknown. We show that the acquired C-domain of CRTDel52 mediates both Mpl binding and disulfide-linked CRTDel52 dimerization. Cysteine mutations within the novel C-domain (C400A and C404A) and the conserved N-terminal domain (N-domain; C163A) of CRTDel52 are required to reduce disulfide-mediated dimers and multimers of CRTDel52. Based on these data and published structures of CRT oligomers, we identify an N-domain dimerization interface relevant to both WT CRT and CRTDel52. Elimination of disulfide bonds and ionic interactions at both N-domain and C-domain dimerization interfaces is required to abrogate the ability of CRTDel52 to mediate cell proliferation via Mpl. Thus, MPNs exploit a natural dimerization interface of CRT combined with C-domain gain of function to achieve cell transformation.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f9/fb/JCB_202009179.PMC8085772.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38916259","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: 8

Elimination of nurse cell nuclei that shuttle into oocytes during oogenesis. 卵形成过程中进入卵母细胞的乳细胞核的消除。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-05 DOI: 10.1083/jcb.202012101

Zehra Ali-Murthy, Richard D Fetter, Wanpeng Wang, Bin Yang, Loic A Royer, Thomas B Kornberg

引用次数: 3

MyD88 oligomer size functions as a physical threshold to trigger IL1R Myddosome signaling. MyD88寡聚物大小作为触发IL1R Myddosome信号的物理阈值。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-06 DOI: 10.1083/jcb.202012071

Rafael Deliz-Aguirre, Fakun Cao, Fenja H U Gerpott, Nichanok Auevechanichkul, Mariam Chupanova, YeVin Mun, Elke Ziska, Marcus J Taylor

{"title":"MyD88 oligomer size functions as a physical threshold to trigger IL1R Myddosome signaling.","authors":"Rafael Deliz-Aguirre, Fakun Cao, Fenja H U Gerpott, Nichanok Auevechanichkul, Mariam Chupanova, YeVin Mun, Elke Ziska, Marcus J Taylor","doi":"10.1083/jcb.202012071","DOIUrl":"https://doi.org/10.1083/jcb.202012071","url":null,"abstract":"A recurring feature of innate immune receptor signaling is the self-assembly of signaling proteins into oligomeric complexes. The Myddosome is an oligomeric complex that is required to transmit inflammatory signals from TLR/IL1Rs and consists of MyD88 and IRAK family kinases. However, the molecular basis for how Myddosome proteins self-assemble and regulate intracellular signaling remains poorly understood. Here, we developed a novel assay to analyze the spatiotemporal dynamics of IL1R and Myddosome signaling in live cells. We found that MyD88 oligomerization is inducible and initially reversible. Moreover, the formation of larger, stable oligomers consisting of more than four MyD88s triggers the sequential recruitment of IRAK4 and IRAK1. Notably, genetic knockout of IRAK4 enhanced MyD88 oligomerization, indicating that IRAK4 controls MyD88 oligomer size and growth. MyD88 oligomer size thus functions as a physical threshold to trigger downstream signaling. These results provide a mechanistic basis for how protein oligomerization might function in cell signaling pathways.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8105725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38956418","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: 14

TRIM37 prevents formation of condensate-organized ectopic spindle poles to ensure mitotic fidelity. TRIM37防止形成凝聚组织异位纺锤杆，以确保有丝分裂的保真度。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-13 DOI: 10.1083/jcb.202010180

Franz Meitinger, Dong Kong, Midori Ohta, Arshad Desai, Karen Oegema, Jadranka Loncarek

{"title":"TRIM37 prevents formation of condensate-organized ectopic spindle poles to ensure mitotic fidelity.","authors":"Franz Meitinger, Dong Kong, Midori Ohta, Arshad Desai, Karen Oegema, Jadranka Loncarek","doi":"10.1083/jcb.202010180","DOIUrl":"https://doi.org/10.1083/jcb.202010180","url":null,"abstract":"Centrosomes are composed of a centriolar core surrounded by pericentriolar material that nucleates microtubules. The ubiquitin ligase TRIM37 localizes to centrosomes, but its centrosomal roles are not yet defined. We show that TRIM37 does not control centriole duplication, structure, or the ability of centrioles to form cilia but instead prevents assembly of an ectopic centrobin-scaffolded structured condensate that forms by budding off of centrosomes. In ∼25% of TRIM37-deficient cells, the condensate organizes an ectopic spindle pole, recruiting other centrosomal proteins and acquiring microtubule nucleation capacity during mitotic entry. Ectopic spindle pole-associated transient multipolarity and multipolar segregation in TRIM37-deficient cells are suppressed by removing centrobin, which interacts with and is ubiquitinated by TRIM37. Thus, TRIM37 ensures accurate chromosome segregation by preventing the formation of centrobin-scaffolded condensates that organize ectopic spindle poles. Mutations in TRIM37 cause the disorder mulibrey nanism, and patient-derived cells harbor centrobin condensate-organized ectopic poles, leading us to propose that chromosome missegregation is a pathological mechanism in this disorder.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/02/72/JCB_202010180.PMC8127006.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38895469","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: 6

Chromosome oscillation promotes Aurora A-dependent Hec1 phosphorylation and mitotic fidelity. 染色体振荡促进Aurora a依赖性的Hec1磷酸化和有丝分裂保真度。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 Epub Date: 2021-05-14 DOI: 10.1083/jcb.202006116

Kenji Iemura, Toyoaki Natsume, Kayoko Maehara, Masato T Kanemaki, Kozo Tanaka

{"title":"Chromosome oscillation promotes Aurora A-dependent Hec1 phosphorylation and mitotic fidelity.","authors":"Kenji Iemura, Toyoaki Natsume, Kayoko Maehara, Masato T Kanemaki, Kozo Tanaka","doi":"10.1083/jcb.202006116","DOIUrl":"https://doi.org/10.1083/jcb.202006116","url":null,"abstract":"Most cancer cells show chromosomal instability, a condition where chromosome missegregation occurs frequently. We found that chromosome oscillation, an iterative chromosome motion during metaphase, is attenuated in cancer cell lines. We also found that metaphase phosphorylation of Hec1 at serine 55, which is mainly dependent on Aurora A on the spindle, is reduced in cancer cell lines. The Aurora A-dependent Hec1-S55 phosphorylation level was regulated by the chromosome oscillation amplitude and vice versa: Hec1-S55 and -S69 phosphorylation by Aurora A is required for efficient chromosome oscillation. Furthermore, enhancement of chromosome oscillation reduced the number of erroneous kinetochore-microtubule attachments and chromosome missegregation, whereas inhibition of Aurora A during metaphase increased such errors. We propose that Aurora A-mediated metaphase Hec1-S55 phosphorylation through chromosome oscillation, together with Hec1-S69 phosphorylation, ensures mitotic fidelity by eliminating erroneous kinetochore-microtubule attachments. Attenuated chromosome oscillation and the resulting reduced Hec1-S55 phosphorylation may be a cause of CIN in cancer cell lines.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/18/7d/JCB_202006116.PMC8129796.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38912182","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: 14

O-GlcNAc modification of nuclear pore complexes accelerates bidirectional transport. O-GlcNAc修饰核孔复合物加速了双向运输。

IF 7.8

The Journal of Cell Biology Pub Date : 2021-07-05 DOI: 10.1083/jcb.202010141

Tae Yeon Yoo, Timothy J Mitchison

{"title":"O-GlcNAc modification of nuclear pore complexes accelerates bidirectional transport.","authors":"Tae Yeon Yoo, Timothy J Mitchison","doi":"10.1083/jcb.202010141","DOIUrl":"https://doi.org/10.1083/jcb.202010141","url":null,"abstract":"Macromolecular transport across the nuclear envelope depends on facilitated diffusion through nuclear pore complexes (NPCs). The interior of NPCs contains a permeability barrier made of phenylalanine-glycine (FG) repeat domains that selectively facilitates the permeation of cargoes bound to nuclear transport receptors (NTRs). FG-repeat domains in NPCs are a major site of O-linked N-acetylglucosamine (O-GlcNAc) modification, but the functional role of this modification in nucleocytoplasmic transport is unclear. We developed high-throughput assays based on optogenetic probes to quantify the kinetics of nuclear import and export in living human cells. We found that increasing O-GlcNAc modification of the NPC accelerated NTR-facilitated transport of proteins in both directions, and decreasing modification slowed transport. Superresolution imaging revealed strong enrichment of O-GlcNAc at the FG-repeat barrier. O-GlcNAc modification also accelerated passive permeation of a small, inert protein through NPCs. We conclude that O-GlcNAc modification accelerates nucleocytoplasmic transport by enhancing the nonspecific permeability of the FG-repeat barrier, perhaps by steric inhibition of interactions between FG repeats.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2021-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fb/2f/JCB_202010141.PMC8091080.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38836849","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