International Journal of Biochemistry & Cell Biology最新文献

{"title":"Aminoadipic acid aggravates atherosclerotic vascular inflammation through ROS/TXNIP/NLRP3 pathway, a harmful microbial metabolite reduced by paeonol","authors":"Tian Wang ,&nbsp;Hongfei Wu ,&nbsp;Xiaoyan Shi ,&nbsp;Min Dai ,&nbsp;Yarong Liu","doi":"10.1016/j.biocel.2024.106678","DOIUrl":"10.1016/j.biocel.2024.106678","url":null,"abstract":"<div><h3>Aim</h3><div>Our previous study has found a differential microbial metabolite in atherosclerosis (AS) mice, aminoadipic acid (AAA), which was considered as a potential harmful metabolite. However, whether it can promote AS vascular inflammation and its mechanisms remain unclear. Paeonol (Pae) plays an anti-AS role by regulating the metabolic profile, but whether Pae exerts its antiatherogenic effect by reducing serum AAA levels is unknown.</div></div><div><h3>Results</h3><div>The clinical trial results showed that the AS patients’ serum AAA levels were higher than those healthy people’. Besides, AAA supplementation could increase aortic plaque size, serum inflammatory cytokines levels and liver malondialdehyde, superoxide dismutase levels in AS mice. Moreover, after AAA stimulation, the ROS levels and ASC, TXNIP, NLRP3 and caspase-1 proteins levels were increased in HUVECs, which could be reversed by antioxidant NAC and NLRP3 inhibitor. Pae significantly reduced the plaque size in the aorta, improved blood lipid levels and decreased serum inflammation factor levels in AS mice. Simultaneously, Pae could reduce the serum AAA levels of AS mice through the gut microbiota transmission. Finally, Pae inhibited NLRP3 inflammasome activation in aortas of AS mice. Broad-spectrum antibiotics could weaken the inhibitory effect of Pae on NLRP3 inflammasome.</div></div><div><h3>Conclusion</h3><div>Our study clarified that AAA could promote AS vascular inflammation via activating the ROS/TXNIP/NLRP3 pathway. Pae could inhibit AS development by reducing serum AAA levels in a microbiota-dependent manner. Taken together, we proposed that AAA could be served as a potential biomarker for AS clinical diagnosis and provided a new treatment strategy for AS.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106678"},"PeriodicalIF":3.4,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142554306","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":"The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium","authors":"Nektarios Barabutis,&nbsp;Saikat Fakir","doi":"10.1016/j.biocel.2024.106679","DOIUrl":"10.1016/j.biocel.2024.106679","url":null,"abstract":"<div><div>The endothelium forms a monolayer, which functions to ensure tissue homeostasis. Barrier hyperpermeability has been associated with lung, brain and eye disease. An emerging body of evidence reports the involvement of Never-in-Mitosis A - Related Kinases in vascular responses, suggesting their value as potential therapeutic targets in endothelial-dependent disorders.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106679"},"PeriodicalIF":3.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512230","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":"ASPSCR1::TFE3-mediated upregulation of insulin receptor substrate 2 (IRS-2) activates PI3K/AKT signaling and promotes malignant phenotype","authors":"Naoko Ishiguro,&nbsp;Mayumi Nakagawa","doi":"10.1016/j.biocel.2024.106676","DOIUrl":"10.1016/j.biocel.2024.106676","url":null,"abstract":"<div><div>The <em>ASPSCR1::TFE3</em> fusion gene, resulting from chromosomal translocation, is detected in alveolar soft part sarcoma (ASPS) and a subset of renal cell carcinomas (RCC). The ASPSCR1::TFE3 oncoprotein, functioning as an aberrant transcription factor, contributes to tumor development and progression by inappropriately upregulating target genes. Here, we identified insulin receptor substrate 2 (IRS-2), a cytoplasmic adaptor protein, as a novel transcriptional target of ASPSCR1::TFE3. Ectopic expression of ASPSCR1::TFE3 led to increased IRS-2 mRNA and protein levels. Chromatin immunoprecipitation and luciferase assays demonstrated that ASPSCR1::TFE3 bound to the <em>IRS-2</em> promoter region and enhanced its transcription. Moreover, IRS-2 was highly expressed in the ASPSCR1::TFE3-positive RCC cell line FU-UR1, while small interfering RNA-mediated depletion of ASPSCR1::TFE3 markedly decreased IRS-2 mRNA and protein levels. Functionally, IRS-2 knockdown attenuated activation of the PI3K/AKT pathway and reduced proliferation, migration, invasion, adhesion, and clonogenicity in FU-UR1 cells. Pharmacological inhibition of IRS-2 also reduced AKT activation as well as cell viability, clonogenicity, migration, invasion, and adhesion. These findings suggest that IRS-2, regulated by ASPSCR1::TFE3, promotes tumor progression by activating PI3K/AKT signaling and enhancing the malignant phenotype.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106676"},"PeriodicalIF":3.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479638","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":"Paeoniflorin regulates microglia-astrocyte crosstalk, inhibits inflammatory response, and alleviates neuropathic pain through HSP90AA1/HMGB1 signaling pathway","authors":"Fengqin Luo ,&nbsp;Juan Zhang ,&nbsp;Yunfei Miao ,&nbsp;Danhong Wu ,&nbsp;Hongxia Shen ,&nbsp;Man Lu","doi":"10.1016/j.biocel.2024.106675","DOIUrl":"10.1016/j.biocel.2024.106675","url":null,"abstract":"<div><div>Given the unclear, complex pathogenesis of neuropathic pain and the potential of paeoniflorin in relieving neuropathic pain, this study aimed to further clarify the therapeutic effect of paeoniflorin on neuropathic pain and to preliminarily explore the possible protective mechanisms of paeoniflorin. Chronic constrictive injury-induced Sprague Dawley rats and lipopolysaccharide-induced BV-2 cells were used for <em>in vivo</em> and <em>in vitro</em> experiments, respectively. The exosome uptake assay of mouse astrocytes (PKH-67 fluorescent labeling) and the mechanical nociceptive assay (the von Frey fibrous filaments) were performed. The effects of paeoniflorin and its downstream mechanisms on microglial and astrocyte activation, inflammation-associated proteins and exosome marker were determined. Paeoniflorin alleviated mechanical abnormal pain, decreased levels of ionized calcium binding adapter molecule-1 (Iba-1), glial fibrillary acidic protein, Heat Shock Protein 90 Alpha Family Class A Member 1 (HSP90AA1, inflammatory factor) and High Mobility Group Box 1 (HMGB1, inflammation-related protein), and inhibited neuronal apoptosis in chronic constrictive injury rats or lipopolysaccharide-induced BV-2 cells. However, these effects were offset by HSP90AA1 overexpression in lipopolysaccharide-induced BV-2 cells. Exosomes of BV-2 cells could be absorbed by mouse astrocytes. In addition, HSP90AA1 overexpression reversed the effects of paeoniflorin on HMGB1 expression and inflammatory factors and proteins in mouse astrocytes co-cultured with exosome. Collectively, paeoniflorin alleviates neuropathic pain and inhibits inflammatory responses in chronic constrictive injury by modulating microglia-astrocyte crosstalk through HSP90AA1/HMGB1 pathways, which further evidences the potential of paeoniflorin in the treatment of neuropathic pain.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106675"},"PeriodicalIF":3.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479640","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":"Alteration of N-glycosylation of CDON promotes H2O2-induced DNA damage in H9c2 cardiomyocytes","authors":"Liping Chen ,&nbsp;Hongfei Liu ,&nbsp;Wenxing Zhan ,&nbsp;Changkun Long ,&nbsp;Fang Xu ,&nbsp;Xueer Li ,&nbsp;Xiao-Li Tian ,&nbsp;Shenghan Chen","doi":"10.1016/j.biocel.2024.106671","DOIUrl":"10.1016/j.biocel.2024.106671","url":null,"abstract":"<div><div>Protein glycosylation is involved in DNA damage. Recently, DNA damage has been connected with the pathogenesis of heart failure. Cell adhesion associated, oncogene regulated (CDON), considered as an N-linked glycoprotein, is a transmembrane receptor for modulating cardiac function. But the role of CDON and its glycosylation in DNA damage remains unknown. In this study, we found that the knockdown of CDON caused DNA double-strand breaks as indicated by an increase in phosphorylated histone H2AX (γH2AX) protein level, immunofluorescent intensity of γH2AX and tail DNA moment in H9c2 cardiomyocytes. Conversely, overexpression of CDON led to decreasing DNA damage induced by hydrogen peroxide (H₂O₂) and upregulating the expression of genes related to DNA repair pathways-homologous recombination (HR) and non-homologous end joining (NHEJ). Moreover, we expressed nine predicted N-glycosylation site mutants in H9c2 cells prior to treatment with H₂O₂. The results showed that mutation of N-glycosylation sites (N99Q, N179Q, and N870Q) increased the accumulation of DNA damage and downregulated the expression of HR-related genes, demonstrating that CDON N-glycosylation on DNA damage is site-specific and these specific N-glycan sites may regulate HR repair-related transcript abundance of genes. Our data highlight that N-glycosylation of CDON is critical to cardiomyocyte DNA lesion. It may uncover the potential strategies targeting DNA damage pathway in heart disease.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106671"},"PeriodicalIF":3.4,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401836","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":"A modified model of PANoptosisto identify prognosis and immunotherapy response in bladder cancer","authors":"Weichao Lv ,&nbsp;Xiaohang Lei ,&nbsp;Hongyuan Wang ,&nbsp;Tongtong Wang ,&nbsp;Jianguo Zhang","doi":"10.1016/j.biocel.2024.106672","DOIUrl":"10.1016/j.biocel.2024.106672","url":null,"abstract":"<div><h3>Background</h3><div>Cell death, including apoptosis and necrosis, collectively known as widespread apoptosis. The present study aims to investigate the mechanism of action in widespread apoptosis-related modification patterns in bladder cancer.</div></div><div><h3>Methods</h3><div>Using a clinical genomics database, we obtained transcriptomic data and related clinical information of bladder cancer patients. By employing the least absolute shrinkage analysis, we were able to construct a risk model and single-cell sequencing analysis of differential genes in bladder cancer.</div></div><div><h3>Results</h3><div>Five differentially expressed genes (TMPRSS4, TPST1, FOXD1, ELOVL4, EMP1) associated with widespread apoptosis were identified as features for predicting the prognosis of bladder cancer patients. Survival curve analysis revealed significant differences in prognosis (P&lt;0.05). Additionally, multivariate Cox regression analysis determined the independent risk factor for bladder cancer prognosis as the risk score (P&lt;0.001), with high confidence in the scoring model validated internally (P&lt;0.001). Single-cell sequencing reveals high expression of CDKN2A, ERBB2, and TMPRSS4 in B cells, while HRAS is significantly expressed in fibroblasts.</div></div><div><h3>Conclusion</h3><div>PANscore, as a potential prognostic and immunotherapeutic biomarker, will provide more precise and rational basis for personalized treatment strategies</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106672"},"PeriodicalIF":3.4,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378493","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":"Visualizing, quantifying and mapping chromatin remodelers at work with single-molecule and single-cell imaging","authors":"Hendrik Sielaff ,&nbsp;Ziqing Winston Zhao","doi":"10.1016/j.biocel.2024.106667","DOIUrl":"10.1016/j.biocel.2024.106667","url":null,"abstract":"<div><div>Chromatin remodeling, carried out by four major subfamilies of ATP-dependent remodeler complexes across eukaryotes, alleviates the topological challenge posed by nucleosomes to regulate genome access. Recently, single-molecule and single-cell imaging techniques have been widely employed to probe this crucial process, both <em>in vitro</em> and <em>in cellulo</em>. Herein, we provide an integrated account of key recent efforts that leverage these approaches to visualize, quantify and map chromatin remodelers at work, elucidating diverse aspects of the remodeling process in both space and time, including molecular mechanisms of DNA wrapping/unwrapping, nucleosome translocation and histone exchange, dynamics of chromatin binding/target search and their intranuclear organization into hotspots or phase condensates, as well as functional coupling with transcription. The mechanistic insights and quantitative parameters revealed shed light on a multi-modal yet shared landscape for regulating remodeling across molecular and cellular scales, and pave the way for further interrogating the implications of its misregulation in disease contexts.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106667"},"PeriodicalIF":3.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142373439","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":"MIEN1 on the 17q12 amplicon facilitates the malignant behaviors of gastric cancer via activating IL-6/JAK2/STAT3 pathway","authors":"Jing Lin ,&nbsp;Dong Wang ,&nbsp;Jiahui Zhou ,&nbsp;Jing Bai ,&nbsp;Shouzhen Sun ,&nbsp;Xueyuan Jia ,&nbsp;Xiao Liang ,&nbsp;Songbin Fu ,&nbsp;Jingcui Yu","doi":"10.1016/j.biocel.2024.106666","DOIUrl":"10.1016/j.biocel.2024.106666","url":null,"abstract":"<div><div>Oncogene amplification is a significant factor contributing to poor prognosis and limited treatment in patients with advanced gastric cancer. Therefore, identifying amplified oncogenes and elucidating their oncogenic mechanisms will provide reliable therapeutic targets for the clinical treatment of gastric cancer. In this study, we identify a high amplification of 17q12, which includes five oncogenes that are co-amplified and co-overexpressed with ERBB2 using array comparative genomic hybridization, with migration and invasion enhancer 1 (MIEN1) being particularly highlighted for its clinical significance, function, and role in gastric cancer progression. By detecting MIEN1 copy number and expression level across eight gastric cancer cell lines and in tissue microarrays from 543 primary gastric cancer tissues, we found that MIEN1 amplification and overexpression correlated with sex and Lauren’s intestinal type classification of gastric cancer. Besides that, elevated MIEN1 expression was associated with poorer patient survival. In vitro experiments have shown that MIEN1 overexpression enhanced cell proliferation, invasion, and migration, whereas MIEN1 knockdown reversed these malignant phenotypes in vitro. Furthermore, MIEN1 knockdown inhibited tumorigenesis and metastasis of gastric cancer cells in nude mice. Mechanistically, MIEN1 activates the IL-6/JAK2/STAT3 signaling pathway, which drives the proliferation, invasion, and migration of gastric cancer cells. This study demonstrates that MIEN1 contributes to the malignant behavior of gastric cancer through the IL-6/JAK2/STAT3 pathway, suggesting that MIEN1 could serve as a valuable therapeutic target for gastric cancer.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106666"},"PeriodicalIF":3.4,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331580","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":"Classical psychedelics’ action on brain monoaminergic systems","authors":"Jasmine Jade Butler ,&nbsp;Daria Ricci ,&nbsp;Chloé Aman ,&nbsp;Anna Beyeler ,&nbsp;Philippe De Deurwaerdère","doi":"10.1016/j.biocel.2024.106669","DOIUrl":"10.1016/j.biocel.2024.106669","url":null,"abstract":"<div><div>The study of the mechanism of action of classical psychedelics has gained significant interest due to their clinical potential in the treatment of several psychiatric conditions, including major depressive and anxiety disorders. These drugs bind 5-hydroxytryptamine receptors (5-HTR) including 5-HT_1AR, 5-HT_2AR, 5-HT_2BR, and/or 5-HT₂_CR, as well as other targets. 5-HTRs regulate the activity of ascending monoaminergic neurons, a mechanism primarily involved in the action of classical antidepressant drugs, antipsychotics, and drugs of abuse. Sparse neurochemical data have been produced on the control of monoaminergic neuron activity in response to classical psychedelics. Here we review the available data in order to determine whether classical psychedelics have specific neurochemical effects on serotonergic, dopaminergic, and noradrenergic neurons. The data show that these drugs have disparate effects on each monoaminergic system, demonstrating a complex response with state-dependent and region-specific effects. For instance, several psychedelics inhibit the firing of serotonergic neurons, although this is not necessarily associated with a decrease in serotonin release in all regions. Noradrenergic neuron spontaneous activity also appears to be inhibited by psychedelics, also not necessarily associated with a decrease in noradrenaline release in all regions. Psychedelics influence on dopaminergic systems is also complex as the above-mentioned 5-HTRs may have opposing effects on dopaminergic neuron activity, in a state-dependent manner. There is an apparent lack of clear neuronal signature induced by psychedelics on monoaminergic neuron activity despite specific recurrent mechanisms. This review provides a current summary of the action of psychedelics on monoamine neuromodulators serotonin, dopamine and noradrenaline, compiling reoccurring and contradictory findings demonstrating that a monoamine signature of psychedelics, if applicable, would be state- and region-dependant.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106669"},"PeriodicalIF":3.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331581","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":"SUMOylation of cardiac myosin binding protein-C reduces its phosphorylation and results in impaired relaxation following treatment with isoprenaline","authors":"Alice Main,&nbsp;Sheon Mary,&nbsp;Yuan Yan Sin,&nbsp;Tom A. Wright,&nbsp;Jiayue Ling,&nbsp;Connor M. Blair,&nbsp;Godfrey L. Smith,&nbsp;Will Fuller,&nbsp;George S. Baillie","doi":"10.1016/j.biocel.2024.106668","DOIUrl":"10.1016/j.biocel.2024.106668","url":null,"abstract":"<div><div>Systolic and diastolic functions are coordinated in the heart by myofilament proteins that influence force of contraction and calcium sensitivity. Fine control of these processes is afforded by a variety of post-translation modifications that occur on specific proteins at different times during each heartbeat. Cardiac myosin binding protein-C is a sarcomeric accessory protein whose function is to interact transiently with actin, tropomyosin and myosin. Previously many different types of post-translational modification have been shown to influence the action of myosin binding protein-C and we present the first report that the protein can be modified covalently by the small ubiquitin like modifier protein tag. Analysis by mass spectrometry suggests that there are multiple modification sites on myosin binding protein-C for this tag and single point mutations did not serve to abolish the covalent addition of the small ubiquitin like modifier protein. Functionally, our data from both model human embryonic kidney cells and transfected neonatal cardiac myocytes suggests that the modification reduces phosphorylation of the filament protein on serine 282. In cardiac myocytes, the hypo-phosphorylation coincided with a significantly slower relaxation response following isoprenaline induced contraction. We hypothesise that this novel modification of myosin binding protein-C represents a new level of control that acts to alter the relaxation kinetics of cardiac myocytes.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106668"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001602/pdfft?md5=ae25804bd223f4802b2c4f103ab4ecbd&pid=1-s2.0-S1357272524001602-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315066","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}