Journal of cellular biochemistry最新文献

{"title":"RETRACTION to “Adipose Tissue-Derived Stem Cells Inhibit Hypertrophic Scar (HS) Fibrosis via p38/MAPK Pathway”","authors":"","doi":"10.1002/jcb.30689","DOIUrl":"10.1002/jcb.30689","url":null,"abstract":"<p><b>RETRACTION</b>: C.-Y. Chai, J. Song, Z. Tan, I.-C. Tai, C. Zhang, and S. Sun, “Adipose Tissue-Derived Stem Cells Inhibit Hypertrophic Scar (HS) Fibrosis via p38/MAPK Pathway,” <i>Journal of Cellular Biochemistry</i> 120, no. 3 (2019): 4057–4064, https://doi.org/10.1002/jcb.27689.</p><p>The above article, published online on 27 September 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, multiple image elements in Figures 1, 2, 3, and 4 were found to have been previously published by different author groups. Accordingly, the conclusions of this article are considered invalid by the editors.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30689","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800130","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}

{"title":"Intrinsic Factors Behind the Long-COVID: V. Immunometabolic Disorders","authors":"Muhamed Adilović,&nbsp;Altijana Hromić-Jahjefendić,&nbsp;Lejla Mahmutović,&nbsp;Jasmin Šutković,&nbsp;Alberto Rubio-Casillas,&nbsp;Elrashdy M. Redwan,&nbsp;Vladimir N. Uversky","doi":"10.1002/jcb.30683","DOIUrl":"10.1002/jcb.30683","url":null,"abstract":"<div>\u0000 \u0000 <p>The complex link between COVID-19 and immunometabolic diseases demonstrates the important interaction between metabolic dysfunction and immunological response during viral infections. Severe COVID-19, defined by a hyperinflammatory state, is greatly impacted by underlying chronic illnesses aggravating the cytokine storm caused by increased levels of Pro-inflammatory cytokines. Metabolic reprogramming, including increased glycolysis and altered mitochondrial function, promotes viral replication and stimulates inflammatory cytokine production, contributing to illness severity. Mitochondrial metabolism abnormalities, strongly linked to various systemic illnesses, worsen metabolic dysfunction during and after the pandemic, increasing cardiovascular consequences. Long COVID-19, defined by chronic inflammation and immune dysregulation, poses continuous problems, highlighting the need for comprehensive therapy solutions that address both immunological and metabolic aspects. Understanding these relationships shows promise for effectively managing COVID-19 and its long-term repercussions, which is the focus of this review paper.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785406","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}

{"title":"PPARδ Antagonist Inhibited CD47 Expression and Phagocytosis","authors":"Yilei Guo,&nbsp;Bibimaryam Khan,&nbsp;Juanjuan Shi,&nbsp;Yongzhong Hou","doi":"10.1002/jcb.30685","DOIUrl":"10.1002/jcb.30685","url":null,"abstract":"<div>\u0000 \u0000 <p>Increasing evidence suggests that CD47 is highly expressed in multiple types of cancer, which could bind to SIRPα on macrophage, leading to inhibition of macrophage phagocytosis and promotion of tumor growth. However, the regulatory mechanism of CD47 gene expression is not completely clear. Our results indicated that colon cancer cells treated with GSK0660 drug, which is one of the PPARδ antagonists, significantly reduced CD47 gene and protein expression levels in a time and dose-dependent manner. CD47 reporter plasmid was constructed and dual-luciferase analysis was performed. The results suggest that GSK0660 treatment markedly reduced CD47 gene transcriptional activity. Moreover, co-cultured analysis showed that GSK0660 treatment increased phagocytosis. BALB/C mice implanted with CT-26 colon cancer cells were treated with GSK0660, and the results showed that GSK0660 significantly inhibited tumor growth. Moreover, the combination of CD47 monoclonal antibody with GSK0660 drug significantly inhibited tumor growth compared to GSK0660 or CD47 antibody treatment alone. These findings suggest that GSK0660 synergized with CD47 antibody to enhance antitumor immunotherapy.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142780047","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}

{"title":"RETRACTION: Upregulation of LncRNA SnoRNA Host Gene 6 Regulates NUAK Family SnF1-like Kinase-1 Expression by Competitively Binding MicroRNA-125b and Interacting with Snail1/2 in Bladder Cancer","authors":"","doi":"10.1002/jcb.30676","DOIUrl":"10.1002/jcb.30676","url":null,"abstract":"<p><b>RETRACTION:</b> C. Wang, W. Tao, S. Ni, Q. Chen, “Upregulation of LncRNA SnoRNA Host Gene 6 Regulates NUAK Family SnF1-like Kinase-1 Expression by Competitively Binding MicroRNA-125b and Interacting with Snail1/2 in Bladder Cancer,” <i>Journal of Cellular Biochemistry</i> 120, no. 1 (2019): 357-367, https://doi.org/10.1002/jcb.27387.</p><p>The above article, published online on 30 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed to concerns raised by third parties on the data presented in the article. Specifically, multiple image elements in Figures 1c, 2c, 2e, 3a, 3b, and 3c were found to have been published elsewhere and in a different scientific context. Accordingly, the editors consider the conclusions of this article to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 12","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30676","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769305","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}

{"title":"Molecular Mechanisms of Curdlan-Induced Suppression of NFATc1 Expression in Osteoclasts","authors":"Ayaka Koga,&nbsp;Yoshie Nagai-Yoshioka,&nbsp;Ryota Yamasaki,&nbsp;Yoshiyuki Adachi,&nbsp;Wataru Fujii,&nbsp;Wataru Ariyoshi","doi":"10.1002/jcb.30682","DOIUrl":"10.1002/jcb.30682","url":null,"abstract":"<div>\u0000 \u0000 <p>Osteoclasts derived from hematopoietic stem cells express immunoreceptors on their cell surface. Previously, we showed that the β-glucan curdlan suppressed osteoclastogenesis via binding to dectin-1, a pattern recognition receptor. Curdlan negatively regulates osteoclast differentiation and bone resorption capacity by suppressing the expression of nuclear factor of activated T cells 1 (NFATc1), a master factor for osteoclast differentiation, in a dectin-1-dependent manner; however, the mechanism involved in this process has not yet been fully elucidated. In this study, we aimed to elucidate the molecular mechanism involved in the suppression of RANKL-induced osteoclast differentiation by curdlan. Real-time RT-qPCR results showed that curdlan suppressed the expression of NFATc1 in cells of the osteoclast progenitor cell line RAW264.7 overexpressing dectin-1 (d-RAW cells), without altering the expression of negative regulators. Therefore, we examined the effect of curdlan on the NF-κB pathway, which is important for the induction of NFATc1 expression. Western blot analysis results showed that curdlan addition suppressed RANKL-induced NF-κB activation in the vector control line (c-RAW) cells with low expression of dectin-1, in d-RAW cells, and the parental RAW264.7 (RAW) cells. The results of tartrate-resistant alkaline phosphatase staining and real-time RT-qPCR showed that curdlan addition suppressed osteoclast differentiation in RAW cells, suggesting the presence of a dectin-1-independent modification system. Finally, we focused on the complement receptor 3 (CR3), which binds β-glucan, and revealed that blocking the binding of β-glucan to the CD11b molecule, a component of CR3, by neutralizing antibody, recovered the suppression of IκBα degradation by curdlan. These results suggest that the suppression of osteoclast differentiation by curdlan involves not only the dectin-1-dependent pathway but also the negative regulation of NFATc1 via modification of the NF-κB pathway via CR3 recognition. The results of this study may aid to establish treatment methods for metabolic bone diseases and inflammatory bone destruction and to clarify their pathogenesis.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739529","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}

{"title":"Circ-ECH1 May Compete With miR-708-5p to Regulate Ntrk2 in Bronchopulmonary Dysplasia","authors":"Hanrong Cheng,&nbsp;Dongcai Li,&nbsp;Yuming Tang,&nbsp;Tianyong Hu,&nbsp;Benqing Wu","doi":"10.1002/jcb.30678","DOIUrl":"10.1002/jcb.30678","url":null,"abstract":"<div>\u0000 \u0000 <p>Bronchopulmonary dysplasia (BPD) affects patients' quality of life. Circular RNAs participated in BPD. However, circ-ECH1's role in BPD has not been reported yet. This study aimed to explore the role and mechanism of circ-ECH1 in BPD. Hyperoxia-treated type II alveolar epithelial cells (L2 cells) were used as the in vitro BPD model. CCK-8, flow cytometry, and reactive oxygen species (ROS) were used to evaluate cell viability. Fluorescence in situ hybridization confirmed the subcellular localization. Circ-ECH1 overexpression (or inhibited) and miR-708-5p mimics were used to investigate the roles of circ-ECH1 and miR-708-5p in BPD. Quantitative reverse-transcription polymerase reaction (qRT-PCR) detected the expressions of circ-ECH1, miR-708-5p, and neurotrophic receptor tyrosine kinase 2 (Ntrk2). Ntrk2 expression was evaluated by Western blot analysis. Changes in lung tissues were evaluated by hematoxylin and eosin staining. Pulmonary fibrosis was examined by Mason staining. TUNEL staining was performed to evaluate cell apoptosis in lung tissues. RNA sequencing was performed in the lung tissues of BPD rats. The binding between circ-ECH1 and miR-708-5p was confirmed through dual luciferase activity. Hyperoxia reduced cell viability and increased cell apoptosis and ROS accumulation. In addition, hyperoxia decreased the expression levels of circ-ECH1, which is mainly located in the cytoplasm. Circ-ECH1 overexpression increased cell viability but reduced cell apoptosis and ROS accumulation. On the contrary, interference with circ-ECH1 further promoted cell apoptosis and reduced cell activity. Furthermore, circ-ECH1 overexpression reduced the incidence of pulmonary fibrosis and lung cell apoptosis. RNA sequencing, followed by qRT-PCR, confirmed that the expressions of Ntrk2 and miR-708-5p were affected by circ-ECH1. miR-708-5p mimics reversed the role of circ-ECH1 in the BPD. Mechanistically, circ-ECH1 may bind with miR-708-5p to regulate Ntrk2 expression. Circ-ECH1 may compet with miR-708-5p to regulate Ntrk2 expression in BPD. The findings provided a new target for BPD treatment.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716294","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}

{"title":"Reduction of Chemoresistance by Claudin-14-Targeting Peptide in Human Colorectal Cancer Cells","authors":"Yuko Mizukami,&nbsp;Shotaro Hashimoto,&nbsp;Tomoka Ando,&nbsp;Yoshinobu Ishikawa,&nbsp;Hiroaki Eguchi,&nbsp;Yuta Yoshino,&nbsp;Toshiyuki Matsunaga,&nbsp;Nobuhisa Matsuhashi,&nbsp;Akira Ikari","doi":"10.1002/jcb.30675","DOIUrl":"10.1002/jcb.30675","url":null,"abstract":"<div>\u0000 \u0000 <p>The expression of claudins (CLDNs), major components of tight junctions (TJs), is abnormal in various solid tumors. CLDN14 is highly expressed in human colorectal cancer (CRC) tissues and confers chemoresistance. CLDN14 may become a novel therapeutic target for CRC, but CLDN14-targeting drugs have not been developed. Here, we searched for a CLDN14-targeting peptide, which can suppress CLDN14 expression and chemoresistance using human CRC-derived DLD-1 and LoVo cells. Among some short peptides which mimic the second extracellular loop structure of CLDN14, PSGMK most strongly suppressed the protein expression of CLDN14. The mRNA expression of other endogenous TJ components was unchanged by PSGMK. The PSGMK-induced reduction of CLDN14 protein was inhibited by chloroquine, a lysosome inhibitor, and monodansylcadaverine, a clathrin-dependent endocytosis inhibitor, indicating that PSGMK may enhance endocytosis and lysosomal degradation of CLDN14. In a three-dimensional culture model, the oxidative stress was significantly reduced by PSGMK, whereas hypoxia stress was not. Furthermore, the expression levels of nuclear factor erythroid 2-related factor 2, an oxidative stress response factor, and its target genes were decreased by PSGMK. These results suggest that PSGMK relieves stress conditions in spheroids. The cell viability of spheroids was decreased by anticancer drugs such as doxorubicin and oxaliplatin, which was exaggerated by the cotreatment with PSGMK. Our data indicate that CLDN14-targeting peptide, PSGMK has an anti-chemoresistance effect in CRC cells.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675846","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}

{"title":"Solasodine Downregulates ABCB1 Overexpression in Multidrug Resistant Cancer Cells Via Inhibiting Nrf2/Keap1 Signaling Pathway","authors":"Pradhapsingh Bharathiraja,&nbsp;Sugumar Baskar,&nbsp;N. Rajendra Prasad","doi":"10.1002/jcb.30674","DOIUrl":"10.1002/jcb.30674","url":null,"abstract":"<div>\u0000 \u0000 <p>Multidrug-resistant (MDR) cancer cells maintain redox homeostasis to eliminate oxidative stress-mediated cell death. This study explores the effects of solasodine on regulating P-glycoprotein (P-gp) expression through the Nrf2/Keap1 signaling pathway and oxidative stress-induced sensitization of drug-resistant cancer cells to chemotherapeutics. Initially, the oxidative stress indicators such as intracellular ROS generation, the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and gamma-H2AX (γ-H2AX) in the KBChR-8-5 drug-resistant cells were measured. Additionally, the protein expression levels of Nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap1), and ATP Binding Cassette Subfamily B Member 1 (ABCB1)/P-gp were measured at various concentrations of solasodine (1, 5, &amp; 10 µM) through immunofluorescence and western blot analysis. The antioxidant activities in the KBChR-8-5 cells were assessed using established protocols. In this investigation, the treatment with solasodine and doxorubicin combination showed a notable increase in intracellular ROS generation in KBChR-8-5 cells. Furthermore, this combination treatment led to enhanced nuclear condensation, elevated levels of 8-OHdG, and increased γ-H2AX foci formation in the KBChR-8-5 cells. Solasodine treatment effectively inhibited the nuclear translocation of Nrf2 and activation of the <i>ABCB1</i> gene, consequently preventing overexpression of P-gp in KBChR-8-5 cells. Additionally, the combination therapy increased the lipid peroxidation levels while simultaneously reducing the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the levels of glutathione (GSH). These results demonstrated that solasodine disrupts redox balance, and overcomes drug resistance by downregulating P-gp via regulating Nrf2/Keap1 signaling pathway in MDR cancer cells.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620389","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}

{"title":"Structural and Functional Insight Into YefM–YoeB Complex of Toxin–Antitoxin System From Streptococcus pneumoniae","authors":"Do-Hee Kim,&nbsp;Yong-Chan Lee,&nbsp;Chenglong Jin,&nbsp;Sung-Min Kang,&nbsp;Su-Jin Kang,&nbsp;Hoon-Seok Kang,&nbsp;Bong-Jin Lee","doi":"10.1002/jcb.30672","DOIUrl":"10.1002/jcb.30672","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Streptococcus pneumonia</i> is a Gram-positive and facultative anaerobic bacterium that causes a number of diseases, including otitis media, community-acquired pneumonia, sepsis, and meningitis. With the emergence of antibiotic-resistant strains, there is an urgent need to develop antibiotics with a novel mechanism. The toxin–antitoxin (TA) system, which is primarily found in prokaryotes, consists of a toxin and its equivalent antitoxin genes. The YefM–YoeB module is a Type II TA system, where the YoeB toxin functions as a putative mRNA interferase upon activation, while the YefM antitoxin acts as a transcription repressor by binding to its promoter region along with YoeB. In this study, we determined the crystal structure of the YefM–YoeB complex from <i>S</i>. <i>pneumoniae</i> TIGR4 to comprehend the binding mechanism of the TA system. Furthermore, an in vitro ribonuclease activity assay was conducted to identify the ribonuclease activity of the YoeB toxin. Additionally, furthermore, the oligomeric state of the YefM–YoeB complex in solution was investigated, and a DNA-binding mode was proposed. These structural and functional insights into the YefM–YoeB complex could provide valuable information for the development of novel antibiotics targeting <i>S</i>. <i>pneumonia</i>-associated diseases.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620473","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}

{"title":"RETRACTION: Trans-Cleaving Hammerhead Ribozyme in Specific Regions Can Improve Knockdown Efficiency In Vivo","authors":"","doi":"10.1002/jcb.30677","DOIUrl":"10.1002/jcb.30677","url":null,"abstract":"<p><b>RETRACTION:</b> Y. Peng, X. Ai, and B. Peng, “<i>Trans</i>-cleaving Hammerhead Ribozyme in Specific Regions Can Improve Knockdown Efficiency In Vivo,” <i>Journal of Cellular Biochemistry</i> (Early View): https://doi.org/10.1002/jcb.30249.</p><p>The above article, published online on 11 April 2022 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed upon the authors’ request due to concerns related to the data presented in the article. The authors admitted significant errors in the evaluation of the fluorescence intensity, resulting in inaccurate data on the trans-cleaving efficiency of the presented system. They also informed the journal of errors in the results of the immunoblot assays. As the identified errors affect the overall conclusions of the study, the article is retracted.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 12","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30677","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620374","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}