Journal of cellular biochemistry最新文献

{"title":"RETRACTION: Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats","authors":"","doi":"10.1002/jcb.30622","DOIUrl":"10.1002/jcb.30622","url":null,"abstract":"<p><b>RETRACTION:</b> Z. Zhao, J.-Z. Guan, M. Wu, G.-H. Lai, and Z.-L. Zhu. Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats. <i>Journal of Cellular Biochemistry</i> 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748.</p><p>The above article, published online on 9 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.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. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, the same sample used to depict the immunofluorescence staining in Figure 5B was found to have been used in a different scientific context in a previous publication from a different author group. Thus, the editors consider the conclusions of this article to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30622","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626837","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":"RETRACTION: Methyl Helicterate Inhibits Hepatic Stellate Cell Activation through Downregulating the ERK1/2 Signaling Pathway","authors":"","doi":"10.1002/jcb.30623","DOIUrl":"10.1002/jcb.30623","url":null,"abstract":"<p><b>RETRACTION:</b> Y. Wei, X. Zhang, S. Wen, S. Huang, Q. Huang, S. Lu, F. Bai, J. Nie, J. Wei, Z. Lu, and X. Lin. Methyl Helicterate Inhibits Hepatic Stellate Cell Activation Through Downregulating the ERK1/2 Signaling Pathway. <i>Journal of Cellular Biochemistry</i> 120, no. 9 (2019): 14936-14945, https://doi.org/10.1002/jcb.28756.</p><p>The above article, published online on 22 April 2019 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. Multiple image elements in Figures 2A, 3B, and 4 were found to have been previously published by the same author group in a different scientific context. Furthermore, splicing affecting Figures 5B and 5C has been detected. The authors state that, due to inadequate data management, they were unable to verify whether Figures 2A, 3B, and 4 pertain to this study or to other works, and that Figure 5B and 5C were inappropriately employed. The article is retracted as the editors have lost confidence in the accuracy of the data presented and consider the conclusions of the article to be invalid. The authors agree with the decision to retract the article and would like to extend their sincere apologies for any inconvenience caused.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30623","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626838","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":"Activation of α7 Nicotinic Acetylcholine Receptor Improves Muscle Endurance by Upregulating Orosomucoid Expression and Glycogen Content in Mice","authors":"Fei Chen,&nbsp;Zhen Zhang,&nbsp;Huimin Zhang,&nbsp;Pengyue Guo,&nbsp;Jiayi Feng,&nbsp;Hui Shen,&nbsp;Xia Liu","doi":"10.1002/jcb.30630","DOIUrl":"10.1002/jcb.30630","url":null,"abstract":"<div>\u0000 \u0000 <p>There are presently no acknowledged therapeutic targets or official drugs for the treatment of muscle fatigue. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is expressed in skeletal muscle, with an unknown role in muscle endurance. Here, we try to explore whether α7nAChR could act as a potential therapeutic target for the treatment of muscle fatigue. Results showed that nicotine and PNU-282987 (PNU), as nonspecific and specific agonists of α7nAChR, respectively, could both significantly increase C57BL6/J mice treadmill-running time in a time- and dose-dependent manner. The improvement effect of PNU on running time and ex vivo muscle fatigue index disappeared when α7nAChR deletion. RNA sequencing revealed that the differential mRNAs affected by PNU were enriched in glycolysis/gluconeogenesis signaling pathways. Further studies found that PNU treatment significantly elevates glycogen content and ATP level in the muscle tissues of α7nAChR^+/+ mice but not α7nAChR^-/- mice. α7nAChR activation specifically increased endogenous glycogen-targeting protein orosomucoid (ORM) expression both in vivo skeletal muscle tissues and in vitro C2C12 skeletal muscle cells. In ORM1 deficient mice, the positive effects of PNU on running time, glycogen and ATP content, as well as muscle fatigue index, were abolished. Therefore, the activation of α7nAChR could enhance muscle endurance via elevating endogenous anti-fatigue protein ORM and might act as a promising therapeutic strategy for the treatment of muscle fatigue.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626835","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":"Effect of Oridonin on Experimental Animal Model of Bronchopulmonary Dysplasia","authors":"Shanshan Zhang,&nbsp;Junfu Wang,&nbsp;Zhihong Xin,&nbsp;Chao Sun,&nbsp;Zhiye Ju,&nbsp;Xia Xue,&nbsp;Wen Jiang,&nbsp;Qian Xin,&nbsp;Jue Wang,&nbsp;Zhaohua Zhang,&nbsp;Yun Luan","doi":"10.1002/jcb.30632","DOIUrl":"10.1002/jcb.30632","url":null,"abstract":"<div>\u0000 \u0000 <p>Bronchopulmonary dysplasia (BPD) is a serious disease that occurs in premature and low-birth-weight infants. In recent years, the incidence of BPD has not decreased, and there is no effective treatment for it. Oridonin (Ori) is a traditional Chinese medicine with a wide range of biological activities, especially pharmacological and anti-inflammatory. It is well known that inflammation plays a key role in BPD. However, the therapeutic effect of Ori on BPD has not been studied. Therefore, in the present study, we will observe the anti-inflammatory activity of Ori in an experimental animal model of BPD. Here, we showed that Ori could significantly decrease hyperoxia-induced alveolar injury, inhibit neutrophil recruitment, myeloperoxidase concentrations, and release inflammatory factors in BPD neonatal rats. Taken together, the experimental results suggested that Ori can significantly improve BPD in neonatal rats by inhibiting inflammatory response.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626836","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: 3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition","authors":"","doi":"10.1002/jcb.30625","DOIUrl":"10.1002/jcb.30625","url":null,"abstract":"<p><b>RETRACTION:</b> A. Rajabian, H. R. Sadeghnia, A. Hosseini, S. H. Mousavi and M. T. Boroushaki, “3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition,” <i>Journal of Cellular Biochemistry</i> 121, no. 2 (2020): 1778-1789, https://doi.org/10.1002/jcb.29413.</p><p>The above article, published online on 23 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed due to concerns regarding the suspected splicing of western blot bands presented in the Bax panel of Figure 5c. Furthermore, concerns were raised regarding the unexpected similarity of flow cytometry data representing different experiments shown in Figure 5A (Co-treatment with AKBA 2.5 µM panel) and Figure 5B (Glutamate 8 mM panel). Although the authors provided some supporting data, it was not sufficient to alleviate the concerns. As a result, the editors consider the results and conclusion reported in this article unreliable.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30625","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620078","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":"Correction to “Cytokinetic Abscission: Phosphoinositides and ESCRTs Direct the Final Cut”","authors":"","doi":"10.1002/jcb.30626","DOIUrl":"10.1002/jcb.30626","url":null,"abstract":"<p>F. Gulluni, M. Martini, E. Hirsch, “Cytokinetic Abscission: Phosphoinositides and ESCRTs Direct the Final Cut,” <i>Journal of Cellular Biochemistry</i> 118, no. 11 (2017): 3561–3568, https://doi.org/10.1002/jcb.26066.</p><p>The authors hereby recognize that in writing the article above, they did not adequately acknowledge the significant contributions of sources [<span>1</span>] and [<span>2</span>], which profoundly influenced the shaping of the content of the article.</p><p>The compilation of this review benefited substantially from the insights and research provided by the aforementioned sources and the authors regret any oversight in properly attributing the influence of these sources within the text of their article.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30626","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616525","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":"Let‑7f‑5p Regulated by Hsa_circ_0000437 Ameliorates Bleomycin-Induced Skin Fibrosis","authors":"Baiting Liu,&nbsp;Chenxi Li,&nbsp;Yunyao Bo,&nbsp;Guiping Tian,&nbsp;Lijun Yang,&nbsp;Jianjun Si,&nbsp;Lin Zhang,&nbsp;Yuan Yan","doi":"10.1002/jcb.30629","DOIUrl":"10.1002/jcb.30629","url":null,"abstract":"<div>\u0000 \u0000 <p>The current treatment of skin fibrosis is limited in its effectiveness due to a lack of understanding of the underlying mechanisms. Previous research has shown a connection between microRNAs (miRNAs) and the development of skin fibrosis. Therefore, investigating miRNA for the treatment of skin fibrotic diseases is highly important and merits further exploration. In this study, we have discovered that let-7f-5p could suppress the proliferation, migration, and expression of collagen type I alpha 1 (COL1A1) in human dermal fibroblasts (HDFs). It was further determined that let-7f-5p could target thrombospondin-1 (THBS1), thereby inhibiting the TGF-β2/Smad3 signaling pathway and exerting its biological effects. Additionally, let-7f-5p is regulated by Hsa_circ_0000437, which acts as a sponge molecule for let-7f-5p and consequently regulates the biological function of HDFs. Furthermore, our findings indicate that in vivo overexpression of let-7f-5p leads to a reduction in dermal thickness and COL1A1 expression, effectively inhibiting the progression of bleomycin (BLM)-induced skin fibrosis in mice. Hence, our research enhances the comprehension of the Hsa_circ_0000437/let-7f-5p/THBS1/TGF-β2/Smad3 regulatory network, highlighting the potential of let-7f-5p as a therapeutic approach for the treatment of skin fibrosis.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616526","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":"SARS-CoV-2 Spike Protein Induces Time-Dependent CTSL Upregulation in HeLa Cells and Alveolarspheres","authors":"Magdalena M. Bolsinger,&nbsp;Alice Drobny,&nbsp;Sibylle Wilfling,&nbsp;Stephanie Reischl,&nbsp;Florian Krach,&nbsp;Raul Moritz,&nbsp;Denise Balta,&nbsp;Ute Hehr,&nbsp;Elisabeth Sock,&nbsp;Florian Bleibaum,&nbsp;Frank Hanses,&nbsp;Beate Winner,&nbsp;Susy Prieto Huarcaya,&nbsp;Philipp Arnold,&nbsp;Friederike Zunke","doi":"10.1002/jcb.30627","DOIUrl":"10.1002/jcb.30627","url":null,"abstract":"<p>Autophagy and lysosomal pathways are involved in the cell entry of SARS-CoV-2 virus. To infect the host cell, the spike protein of SARS-CoV-2 binds to the cell surface receptor angiotensin-converting enzyme 2 (ACE2). To allow the fusion of the viral envelope with the host cell membrane, the spike protein has to be cleaved. One possible mechanism is the endocytosis of the SARS-CoV-2–ACE2 complex and subsequent cleavage of the spike protein, mainly by the lysosomal protease cathepsin L. However, detailed molecular and dynamic insights into the role of cathepsin L in viral cell entry remain elusive. To address this, HeLa cells and iPSC-derived alveolarspheres were treated with recombinant SARS-CoV-2 spike protein, and the changes in mRNA and protein levels of cathepsins L, B, and D were monitored. Additionally, we studied the effect of cathepsin L deficiency on spike protein internalization and investigated the influence of the spike protein on cathepsin L promoters in vitro. Furthermore, we analyzed variants in the genes coding for cathepsin L, B, D, and ACE2 possibly associated with disease progression using data from Regeneron's COVID Results Browser and our own cohort of 173 patients with COVID-19, exhibiting a variant of <i>ACE2</i> showing significant association with COVID-19 disease progression. Our in vitro studies revealed a significant increase in cathepsin L mRNA and protein levels following exposure to the SARS-CoV-2 spike protein in HeLa cells, accompanied by elevated mRNA levels of cathepsin B and D in alveolarspheres. Moreover, an increase in cathepsin L promoter activity was detected in vitro upon spike protein treatment. Notably, the knockout of cathepsin L resulted in reduced internalization of the spike protein. The study highlights the importance of cathepsin L and lysosomal proteases in the SARS-CoV-2 spike protein internalization and suggests the potential of lysosomal proteases as possible therapeutic targets against COVID-19 and other viral infections.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30627","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141544872","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":"14-3-3 Family of Proteins: Biological Implications, Molecular Interactions, and Potential Intervention in Cancer, Virus and Neurodegeneration Disorders","authors":"Zheng Yao Low,&nbsp;Ashley Jia Wen Yip,&nbsp;Alvin Man Lung Chan,&nbsp;Wee Sim Choo","doi":"10.1002/jcb.30624","DOIUrl":"10.1002/jcb.30624","url":null,"abstract":"<p>The 14-3-3 family of proteins are highly conserved acidic eukaryotic proteins (25–32 kDa) abundantly present in the body. Through numerous binding partners, the 14-3-3 is responsible for many essential cellular pathways, such as cell cycle regulation and gene transcription control. Hence, its dysregulation has been linked to the onset of critical illnesses such as cancers, neurodegenerative diseases and viral infections. Interestingly, explorative studies have revealed an inverse correlation of 14-3-3 protein in cancer and neurodegenerative diseases, and the direct manipulation of 14-3-3 by virus to enhance infection capacity has dramatically extended its significance. Of these, COVID-19 has been linked to the 14-3-3 proteins by the interference of the SARS-CoV-2 nucleocapsid (N) protein during virion assembly. Given its predisposition towards multiple essential host signalling pathways, it is vital to understand the holistic interactions between the 14-3-3 protein to unravel its potential therapeutic unit in the future. As such, the general structure and properties of the 14-3-3 family of proteins, as well as their known biological functions and implications in cancer, neurodegeneration, and viruses, were covered in this review. Furthermore, the potential therapeutic target of 14-3-3 proteins in the associated diseases was discussed.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30624","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468277","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":"Divergent Biochemical Properties and Disparate Impact of Arrhythmogenic Calmodulin Mutations on Zebrafish Cardiac Function","authors":"Sahar I. Da'as,&nbsp;Angelos Thanassoulas,&nbsp;Brian L. Calver,&nbsp;Alaaeldin Saleh,&nbsp;Doua Abdelrahman,&nbsp;Waseem Hasan,&nbsp;Bared Safieh-Garabedian,&nbsp;Iris Kontogianni,&nbsp;Gheyath K. Nasrallah,&nbsp;George Nounesis,&nbsp;F. Anthony Lai,&nbsp;Michail Nomikos","doi":"10.1002/jcb.30619","DOIUrl":"10.1002/jcb.30619","url":null,"abstract":"<p>Calmodulin (CaM) is a ubiquitous, small cytosolic calcium (Ca²⁺)-binding sensor that plays a vital role in many cellular processes by binding and regulating the activity of over 300 protein targets. In cardiac muscle, CaM modulates directly or indirectly the activity of several proteins that play a key role in excitation-contraction coupling (ECC), such as ryanodine receptor type 2 (RyR2), <span>l</span>-type Ca²⁺ (Ca_v1.2), sodium (NaV1.5) and potassium (KV7.1) channels. Many recent clinical and genetic studies have reported a series of CaM mutations in patients with life-threatening arrhythmogenic syndromes, such as long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT). We recently showed that four arrhythmogenic CaM mutations (N98I, D132E, D134H, and Q136P) significantly reduce the binding of CaM to RyR2. Herein, we investigate in vivo functional effects of these CaM mutations on the normal zebrafish embryonic heart function by microinjecting complementary RNA corresponding to CaM^N98I, CaM^D132E, CaM^D134H, and CaM^Q136P mutants. Expression of CaM^D132E and CaM^D134H mutants results in significant reduction of the zebrafish heart rate, mimicking a severe form of human bradycardia, whereas expression of CaM^Q136P results in an increased heart rate mimicking human ventricular tachycardia. Moreover, analysis of cardiac ventricular rhythm revealed that the CaM^D132E and CaM^N98I zebrafish groups display an irregular pattern of heart beating and increased amplitude in comparison to the control groups. Furthermore, circular dichroism spectroscopy experiments using recombinant CaM proteins reveals a decreased structural stability of the four mutants compared to the wild-type CaM protein in the presence of Ca²⁺. Finally, Ca²⁺-binding studies indicates that all CaM mutations display reduced CaM Ca²⁺-binding affinities, with CaM^D132E exhibiting the most prominent change. Our data suggest that CaM mutations can trigger different arrhythmogenic phenotypes through multiple and complex molecular mechanisms.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30619","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468278","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}