European journal of cell biology最新文献

{"title":"NANOS1 restricts oral cancer cell motility and TGF-ß signaling","authors":"Julia Rosemann ,&nbsp;Jonas Pyko ,&nbsp;Roland Jacob ,&nbsp;Jana Macho ,&nbsp;Matthias Kappler ,&nbsp;Alexander W. Eckert ,&nbsp;Monika Haemmerle ,&nbsp;Tony Gutschner","doi":"10.1016/j.ejcb.2024.151400","DOIUrl":"https://doi.org/10.1016/j.ejcb.2024.151400","url":null,"abstract":"<div><p>Oral squamous cell carcinoma (OSCC) is the most frequent type of cancer of the head and neck area accounting for approx. 377,000 new cancer cases every year. The epithelial-to-mesenchymal transition (EMT) program plays an important role in OSCC progression and metastasis therefore contributing to a poor prognosis in patients with advanced disease. Transforming growth factor beta (TGF-ß) is a powerful inducer of EMT thereby increasing cancer cell aggressiveness. Here, we aimed at identifying RNA-binding proteins (RBPs) that affect TGF-ß-induced EMT. To this end we treated oral cancer cells with TGF-ß and identified a total of 643 significantly deregulated protein-coding genes in response to TGF-ß. Of note, 19 genes encoded RBPs with NANOS1 being the most downregulated RBP. Subsequent cellular studies demonstrated a strong inhibitory effect of NANOS1 on migration and invasion of SAS oral cancer cells. Further mechanistic studies revealed an interaction of NANOS1 with the TGF-ß receptor 1 (TGFBR1) mRNA, leading to increased decay of this transcript and a reduced TGFBR1 protein expression, thereby preventing downstream TGF-ß/SMAD signaling. In summary, we identified NANOS1 as negative regulator of TGF-ß signaling in oral cancer cells.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151400"},"PeriodicalIF":6.6,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000177/pdfft?md5=167b7a8af9a06c0c2500eddda780aba1&pid=1-s2.0-S0171933524000177-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139942605","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":"Immortalised murine R349P desmin knock-in myotubes exhibit a reduced proton leak and decreased ADP/ATP translocase levels in purified mitochondria","authors":"Carolin Berwanger ,&nbsp;Dominic Terres ,&nbsp;Dominik Pesta ,&nbsp;Britta Eggers ,&nbsp;Katrin Marcus ,&nbsp;Ilka Wittig ,&nbsp;Rudolf J. Wiesner ,&nbsp;Rolf Schröder ,&nbsp;Christoph S. Clemen","doi":"10.1016/j.ejcb.2024.151399","DOIUrl":"10.1016/j.ejcb.2024.151399","url":null,"abstract":"<div><p>Desmin gene mutations cause myopathies and cardiomyopathies. Our previously characterised R349P desminopathy mice, which carry the ortholog of the common human desmin mutation R350P, showed marked alterations in mitochondrial morphology and function in muscle tissue. By isolating skeletal muscle myoblasts from offspring of R349P desminopathy and p53 knock-out mice, we established an immortalised cellular disease model. Heterozygous and homozygous R349P desmin knock-in and wild-type myoblasts could be well differentiated into multinucleated spontaneously contracting myotubes. The desminopathy myoblasts showed the characteristic disruption of the desmin cytoskeleton and desmin protein aggregation, and the desminopathy myotubes showed the characteristic myofibrillar irregularities. Long-term electrical pulse stimulation promoted myotube differentiation and markedly increased their spontaneous contraction rate. In both heterozygous and homozygous R349P desminopathy myotubes, this treatment restored a regular myofibrillar cross-striation pattern as seen in wild-type myotubes. High-resolution respirometry of mitochondria purified from myotubes by density gradient ultracentrifugation revealed normal oxidative phosphorylation capacity, but a significantly reduced proton leak in mitochondria from the homozygous R349P desmin knock-in cells. Consistent with a reduced proton flux across the inner mitochondrial membrane, our quantitative proteomic analysis of the purified mitochondria revealed significantly reduced levels of ADP/ATP translocases in the homozygous R349P desmin knock-in genotype. As this alteration was also detected in the soleus muscle of R349P desminopathy mice, which, in contrast to the mitochondria purified from cultured cells, showed a variety of other dysregulated mitochondrial proteins, we consider this finding to be an early step in the pathogenesis of secondary mitochondriopathy in desminopathy.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151399"},"PeriodicalIF":6.6,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000165/pdfft?md5=d463031335b9d8d2f66af0b6b1840115&pid=1-s2.0-S0171933524000165-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139920196","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 naringenin modulation of mitochondrial permeability transition acting on F1FO-ATPase and counteracting saline load-induced injury in SHRSP cerebral endothelial cells","authors":"Salvatore Nesci ,&nbsp;Cristina Algieri ,&nbsp;Matteo Antonio Tallarida ,&nbsp;Rosita Stanzione ,&nbsp;Saverio Marchi ,&nbsp;Donatella Pietrangelo ,&nbsp;Fabiana Trombetti ,&nbsp;Luca D’Ambrosio ,&nbsp;Maurizio Forte ,&nbsp;Maria Cotugno ,&nbsp;Ilaria Nunzi ,&nbsp;Rachele Bigi ,&nbsp;Loredana Maiuolo ,&nbsp;Antonio De Nino ,&nbsp;Paolo Pinton ,&nbsp;Giovanni Romeo ,&nbsp;Speranza Rubattu","doi":"10.1016/j.ejcb.2024.151398","DOIUrl":"https://doi.org/10.1016/j.ejcb.2024.151398","url":null,"abstract":"<div><p>Naringenin (NRG) was characterized for its ability to counteract mitochondrial dysfunction which is linked to cardiovascular diseases. The F₁F_O-ATPase can act as a molecular target of NRG. The interaction of NRG with this enzyme can avoid the energy transmission mechanism of ATP hydrolysis, especially in the presence of Ca²⁺ cation used as cofactor. Indeed, NRG was a selective inhibitor of the hydrophilic F₁ domain displaying a binding site overlapped with quercetin in the inside surface of an annulus made by the three α and the three β subunits arranged alternatively in a hexamer. The kinetic constant of inhibition suggested that NRG preferred the enzyme activated by Ca²⁺ rather than the F₁F_O-ATPase activated by the natural cofactor Mg²⁺. From the inhibition type mechanism of NRG stemmed the possibility to speculate that NRG can prevent the activation of F₁F_O-ATPase by Ca²⁺. The event correlated to the protective role in the mitochondrial permeability transition pore opening by NRG as well as to the reduction of ROS production probably linked to the NRG chemical structure with antioxidant action. Moreover, in primary cerebral endothelial cells (ECs) obtained from stroke prone spontaneously hypertensive rats NRG had a protective effect on salt-induced injury by restoring cell viability and endothelial cell tube formation while also rescuing complex I activity.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151398"},"PeriodicalIF":6.6,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000153/pdfft?md5=44a7a4ec51bf85a8291fe739ca43f7a5&pid=1-s2.0-S0171933524000153-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139749326","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":"Deletion of exons 2 and 3 from Actb and cell immortalization lead to widespread, β-actin independent alterations in gene expression associated with cell cycle control","authors":"Lauren J. Sundby ,&nbsp;William M. Southern ,&nbsp;Jiao Sun ,&nbsp;Xiaobai Patrinostro ,&nbsp;Wei Zhang ,&nbsp;Jeongsik Yong ,&nbsp;James M. Ervasti","doi":"10.1016/j.ejcb.2024.151397","DOIUrl":"10.1016/j.ejcb.2024.151397","url":null,"abstract":"<div><p>The cytoplasmic actin proteins, β- and γ-actin, are 99% identical but thought to perform non-redundant functions. The nucleotide coding regions of cytoplasmic actin genes, <em>Actb</em> and <em>Actg1</em>, are 89% identical. Knockout (KO) of <em>Actb</em> by Cre-mediated deletion of first coding exons 2 and 3 in mice is embryonic lethal and fibroblasts derived from KO embryos (MEFs) fail to proliferate. In contrast, <em>Actg1</em> KO MEFs display with a much milder defect in cell proliferation and <em>Actg1</em> KO mice are viable, but present with increased perinatal lethality. Recent studies have identified important protein-independent functions for both <em>Actb</em> and <em>Actg1</em> and demonstrate that deletions within the <em>Actb</em> nucleotide sequence, and not loss of the β-actin protein, cause the most severe phenotypes in KO mice and cells. Here, we use a multi-omics approach to better understand what drives the phenotypes of <em>Actb</em> KO MEFs. RNA-sequencing and mass spectrometry reveal largescale changes to the transcriptome, proteome, and phosphoproteome in cells lacking <em>Actb</em> but not those only lacking β-actin protein. Pathway analysis of genes and proteins differentially expressed upon <em>Actb</em> KO suggest widespread dysregulation of genes involved in the cell cycle that may explain the severe defect in proliferation.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151397"},"PeriodicalIF":6.6,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000141/pdfft?md5=e1f8394c38e517d78b6126ca98964fca&pid=1-s2.0-S0171933524000141-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139827702","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":"Physico-chemical characterization of the tumour microenvironment of pancreatic ductal adenocarcinoma","authors":"Elena García-Gareta ,&nbsp;Alejandro Calderón-Villalba ,&nbsp;Pilar Alamán-Díez ,&nbsp;Carlos Gracia Costa ,&nbsp;Pedro Enrique Guerrero ,&nbsp;Carlota Mur ,&nbsp;Ana Rueda Flores ,&nbsp;Nerea Olivera Jurjo ,&nbsp;Patricia Sancho ,&nbsp;María Ángeles Pérez ,&nbsp;José Manuel García-Aznar","doi":"10.1016/j.ejcb.2024.151396","DOIUrl":"https://doi.org/10.1016/j.ejcb.2024.151396","url":null,"abstract":"<div><p>Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive lethal malignancy that accounts for more than 90% of pancreatic cancer diagnoses. Our research is focused on the physico-chemical properties of the tumour microenvironment (TME), including its tumoural extracellular matrix (tECM), as they may have an important impact on the success of cancer therapies. PDAC xenografts and their decellularized tECM offer a great material source for research in terms of biomimicry with the original human tumour. Our aim was to evaluate and quantify the physico-chemical properties of the PDAC TME. Both cellularized (native TME) and decellularized (tECM) patient-derived PDAC xenografts were analyzed. A factorial design of experiments identified an optimal combination of factors for effective xenograft decellularization. Our results provide a complete advance in our understanding of the PDAC TME and its corresponding stroma, showing that it presents an interconnected porous architecture with very low permeability and small pores due to the contractility of the cellular components. This fact provides a potential therapeutic strategy based on the therapeutic agent size.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151396"},"PeriodicalIF":6.6,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S017193352400013X/pdfft?md5=81631b39710e7f40425b90c1bf12ebd2&pid=1-s2.0-S017193352400013X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139738358","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":"Thrombospondin 4, a mediator and candidate indicator of pain","authors":"Yanqiong Wu ,&nbsp;Min Yang ,&nbsp;Xueqin Xu ,&nbsp;Yan Gao ,&nbsp;Xiaohui Li ,&nbsp;Yang Li ,&nbsp;Shanchun Su ,&nbsp;Xianqiao Xie ,&nbsp;Zeyong Yang ,&nbsp;Changbin Ke","doi":"10.1016/j.ejcb.2024.151395","DOIUrl":"https://doi.org/10.1016/j.ejcb.2024.151395","url":null,"abstract":"<div><p>Pain is the most common symptom for which patients seek medical attention. Existing treatments for pain control are largely ineffective due to the lack of an accurate way to objectively measure pain intensity and a poor understanding of the etiology of pain. Thrombospondin 4(TSP4), a member of the thrombospondin gene family, is expressed in neurons and astrocytes and induces pain by interacting with the calcium channel alpha-2-delta-1 subunit (Cavα2δ1). In the present study we show that TSP4 expression level correlates positively with pain intensity, suggesting that TSP4 could be a novel candidate of pain indicator. Using RNAi-lentivirus (RNAi-LV) to knock down TSP4 both in vivo and in vitro, together with electrophysiological experiments involving paired patch-clamp recordings of evoked action potentials and post-synaptic currents in cultured neurons, we found that TSP4 contributes to the development of bone cancer pain, neuropathic pain, and inflammatory pain. This effect is mediated by regulation of neuron excitability via inhibition of synapsin I (Syn I) and modulation of excitatory and inhibitory presynaptic transmission via regulation of vesicular glutamate transporter 2(Vglut2), vesicular GABA transporter (VGAT), and glutamate decarboxylase (GAD) expression. The present study provides a replicable, predictive, valid indicator of pain and demonstrated the underlying molecular and electrophysiological mechanisms by which TSP4 contributes to pain.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151395"},"PeriodicalIF":6.6,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000128/pdfft?md5=b8aeb088b41612bf9e0db1b3f579b49c&pid=1-s2.0-S0171933524000128-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139714697","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":"The nexus of nuclear envelope dynamics, circular economy and cancer cell pathophysiology","authors":"Kristina Keuper ,&nbsp;Jiri Bartek ,&nbsp;Apolinar Maya-Mendoza","doi":"10.1016/j.ejcb.2024.151394","DOIUrl":"https://doi.org/10.1016/j.ejcb.2024.151394","url":null,"abstract":"<div><p>The nuclear envelope (NE) is a critical component in maintaining the function and structure of the eukaryotic nucleus. The NE and lamina are disassembled during each cell cycle to enable an open mitosis. Nuclear architecture construction and deconstruction is a prime example of a circular economy, as it fulfills a highly efficient recycling program bound to continuous assessment of the quality and functionality of the building blocks. Alterations in the nuclear dynamics and lamina structure have emerged as important contributors to both oncogenic transformation and cancer progression. However, the knowledge of the NE breakdown and reassembly is still limited to a fraction of participating proteins and complexes. As cancer cells contain highly diverse nuclei in terms of DNA content, but also in terms of nuclear number, size, and shape, it is of great interest to understand the intricate relationship between these nuclear features in cancer cell pathophysiology. In this review, we provide insights into how those NE dynamics are regulated, and how lamina destabilization processes may alter the NE circular economy. Moreover, we expand the knowledge of the lamina-associated domain region by using strategic algorithms, including Artificial Intelligence, to infer protein associations, assess their function and location, and predict cancer-type specificity with implications for the future of cancer diagnosis, prognosis and treatment. Using this approach we identified NUP98 and MECP2 as potential proteins that exhibit upregulation in Acute Myeloid Leukemia (LAML) patients with implications for early diagnosis.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151394"},"PeriodicalIF":6.6,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000116/pdfft?md5=5df94848a0f1ae093e002cd976953089&pid=1-s2.0-S0171933524000116-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139714677","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":"High throughput methods to study protein-protein interactions during host-pathogen interactions","authors":"Giridhar Chandrasekharan,&nbsp;Meera Unnikrishnan","doi":"10.1016/j.ejcb.2024.151393","DOIUrl":"10.1016/j.ejcb.2024.151393","url":null,"abstract":"<div><p>The ability of a pathogen to survive and cause an infection is often determined by specific interactions between the host and pathogen proteins. Such interactions can be both intra- and extracellular and may define the outcome of an infection. There are a range of innovative biochemical, biophysical and bioinformatic techniques currently available to identify protein-protein interactions (PPI) between the host and the pathogen. However, the complexity and the diversity of host-pathogen PPIs has led to the development of several high throughput (HT) techniques that enable the study of multiple interactions at once and/or screen multiple samples at the same time, in an unbiased manner. We review here the major HT laboratory-based technologies employed for host-bacterial interaction studies.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151393"},"PeriodicalIF":6.6,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000104/pdfft?md5=d41c542036c55accba7ce0a2aa219c79&pid=1-s2.0-S0171933524000104-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139554242","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":"Regulation of the HIF switch in human endothelial and cancer cells","authors":"Jakub Slawski ,&nbsp;Maciej Jaśkiewicz ,&nbsp;Anna Barton ,&nbsp;Sylwia Kozioł ,&nbsp;James F. Collawn ,&nbsp;Rafał Bartoszewski","doi":"10.1016/j.ejcb.2024.151386","DOIUrl":"10.1016/j.ejcb.2024.151386","url":null,"abstract":"<div><p>Hypoxia-inducible factors (HIFs) are transcription factors that reprogram the transcriptome for cells to survive hypoxic insults and oxidative stress. They are important during embryonic development and reprogram the cells to utilize glycolysis when the oxygen levels are extremely low. This metabolic change facilitates normal cell survival as well as cancer cell survival. The key feature in survival is the transition between acute hypoxia and chronic hypoxia, and this is regulated by the transition between HIF-1 expression and HIF-2/HIF-3 expression. This transition is observed in many human cancers and endothelial cells and referred to as the HIF Switch. Here we discuss the mechanisms involved in the HIF Switch in human endothelial and cancer cells which include mRNA and protein levels of the alpha chains of the HIFs. A major continuing effort in this field is directed towards determining the differences between normal and tumor cell utilization of this important pathway, and how this could lead to potential therapeutic approaches.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 2","pages":"Article 151386"},"PeriodicalIF":6.6,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000037/pdfft?md5=2ee1e8079d88c9d595cd79d7303ffadd&pid=1-s2.0-S0171933524000037-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139509056","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":"Corrigendum to “Ozone mediates the anticancer effect of air plasma by triggering oxidative cell death caused by H2O2 and iron” [Eur. J. Cell Biol. 102 (2023) 151346]","authors":"M. Suzuki-Karasaki ,&nbsp;Y. Ochiai ,&nbsp;S. Innami ,&nbsp;H. Okajima ,&nbsp;H. Nakayama ,&nbsp;Y. Suzuki-Karasaki","doi":"10.1016/j.ejcb.2024.151385","DOIUrl":"10.1016/j.ejcb.2024.151385","url":null,"abstract":"","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 1","pages":"Article 151385"},"PeriodicalIF":6.6,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933524000025/pdfft?md5=e4d9168fbce927d97576828cdb21e0a3&pid=1-s2.0-S0171933524000025-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139476962","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}