Cell Biochemistry and Function最新文献

{"title":"Effects of p53 on the Regulation of Carbonic Anhydrase 8 in Human Colorectal Cancer Cells: Interaction Between p53 and Sp1","authors":"Jia-Yo Yu,&nbsp;Benjamin Y. Hsieh,&nbsp;Shang-Feng Tsai,&nbsp;Mingli Hsieh","doi":"10.1002/cbf.70081","DOIUrl":"https://doi.org/10.1002/cbf.70081","url":null,"abstract":"<div>\u0000 \u0000 <p>Colorectal cancer ranks among the most common malignancies worldwide. Our previous study indicated Carbonic anhydrase 8 (CA8) is linked to cell proliferation and mobility in colon cancer cells. In the present study, we observed a significant increase in the expression of mutant p53 R273H/P309S in colon cancer cell lines (SW480 and SW620) with stably downregulated CA8. P53, a well-known tumor suppressor gene, is frequently mutated in cancer cells, leading to poor prognosis and drug resistance. Although p53 acts as a transcription factor, the increased mutant p53 did not activate downstream target molecules, suggesting activation defects of mutant p53 R273H/P309S. Furthermore, transient downregulation of CA8 did not alter p53 expression, indicating that the observed increase in mutant p53 in stable cells may be a compensatory effect for cell survival. Given that p53 shares similar consensus sequences at GC-boxes with specific protein 1 (Sp1), a predominant transcription factor for CA8 regulation, we examined the relationship between CA8, p53 and Sp1 in HCT116 and SW620 cells harboring wild-type (WT) or mutant p53, respectively. Notably, transient downregulation of p53 or Sp1 led to a significant decrease in CA8 at both mRNA and protein levels in HCT116 and SW620 cells. Additionally, immunoprecipitation results revealed a protein-protein interaction between Sp1 and p53, suggesting that their interaction may be involved in the regulation of CA8 expression. Although the precise mechanism by which Sp1 and p53 regulate CA8 expression remains unclear, we are the first to report that both Sp1 and p53 are involved in the regulation of the novel <i>hCA8</i> gene. By further unraveling the interplay among CA8, p53, and Sp1, we hope to pave the way for new therapeutic approaches in colon cancer treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085324","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":"Exosomes Derived From BMMSCs Promote B10 Cell Differentiation but Not IL-10 Production","authors":"Jiran Wang,&nbsp;Yingzhi Gu,&nbsp;Jing Wang,&nbsp;Ning Zhang,&nbsp;Xiaozhe Han,&nbsp;Yuxing Bai","doi":"10.1002/cbf.70083","DOIUrl":"https://doi.org/10.1002/cbf.70083","url":null,"abstract":"<div>\u0000 \u0000 <p>The role of IL-10-producing regulatory B cells in inflammatory diseases has recently gained substantial attention. Here, we evaluated the function of mouse bone marrow mesenchymal stem cell-derived exosomes (BMMSC-Exos) and their effect on B-cell differentiation. This study aimed to establish an association between BMMSC-Exos and purified B cells and further explored the anti-inflammatory effect of B10 cells. The expression of inflammatory factors, such as IL-1β, TNF-α, and bone metabolism-related factors, including RANKL, OPG, and secreted IL-10, was investigated by RT-qPCR and ELISA. Populations of CD1d^highCD5⁺ B cells were analyzed by flow cytometry and immunofluorescence. Cell viability was assessed by CCK8 assay. The results showed that when B cells were separated from BMMSCs by Transwell, IL-1β, TNF-α, and RANKL were downregulated, whereas IL-10, OPG/RANKL, and CD1d^highCD5⁺ Breg proportion were upregulated in the cocultured groups. Conversely, when B cells were cultured with BMMSC-Exos, increasing concentrations of exosomes increased the proportion of CD1d^highCD5⁺ and IL-10⁺CD45⁺ Bregs; however, the secretion of both pro-inflammatory cytokines and IL-10 were decreased. We found that BMMSC-Exos induce the differentiation of B cells toward the CD1d^highCD5⁺ and IL-10⁺CD45⁺ Breg phenotype but cannot increase the secretion of IL-10 in vitro.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085295","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":"Hormonal Dynamics of Cervical Cancer: Role of Estrogen and Progesterone","authors":"Jyoti Rani,&nbsp;Seema Yadav,&nbsp;Ritu Yadav,&nbsp;Ravindresh Chhabra","doi":"10.1002/cbf.70082","DOIUrl":"https://doi.org/10.1002/cbf.70082","url":null,"abstract":"<div>\u0000 \u0000 <p>Cervical cancer remains a significant global health burden, with its etiology intricately linked to hormonal influences such as estrogen and progesterone. The effect of estrogen on cervical cancer is dependent upon factors like estrogen receptor subtype and microenvironmental context. Conversely, progesterone has a more complex role, acting as an inducer as well as inhibitor, by coordinating with tumor suppressor genes and cell proliferation markers. Understanding the interplay among these hormones, HPV infection, and cervical carcinogenesis is crucial for improving current preventive strategies and therapeutic interventions. This review outlines the latest insights on how hormones influence cervical cancer development, highlighting their protective and inhibitory effects. It explores the interaction between HPV oncogenes and hormones in cervical cancer progression. Additionally, it consolidates existing knowledge and identifies future research directions, underscoring the potential of hormone modulation as a therapeutic strategy for cervical cancer.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143950217","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":"Disulfidoptosis: A New Key to Unlocking Cancer Treatment","authors":"Xue Li,&nbsp;Shujun Xu,&nbsp;Liwei Jia,&nbsp;Yuan Tian,&nbsp;Xin Meng","doi":"10.1002/cbf.70079","DOIUrl":"https://doi.org/10.1002/cbf.70079","url":null,"abstract":"<div>\u0000 \u0000 <p>The metabolic properties of disulfidoptosis targeting cancer cells have become a new key to unlocking cancer treatment's lock. Conventional cancer therapies aim to kill tumor cells through apoptosis, but cell death is carried out by a network of cascading enzymes. Malignant cells can evade the death process by downregulating key enzymes or inhibiting death-inducing triggers, leading to cancer persistence and recurrence of cancer cells that are resistant to conventional therapies and immune escape, which has compelled researchers to explore new therapeutic avenues. Disulfidoptosis is triggered by the accumulation of excessive intracellular disulfides in cells with high expression of solute carrier family 7 member 11 (SLC7A11) under glucose starvation conditions, which simultaneously induces the breakage of intracellular disulfide bonds and leads to protein malfunction, thereby triggering cancer cell death. However, there is no comprehensive account of disulfidoptosis application in cancer therapy. This review comprehensively summarizes the mechanism of disulfidoptosis for cancer treatment, which provides new ideas for cancer treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143904983","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":"IL-37 Protects Against Ventilator-Induced Lung Injury by Inhibiting NLRP3 Activation","authors":"Xingmeng Xu,&nbsp;Weili Liu,&nbsp;Yan Xu,&nbsp;Yinghong Fan,&nbsp;Fei Han,&nbsp;Jiajia Pan,&nbsp;Guotao Lu,&nbsp;Chenlong Yi,&nbsp;Qingfen Zhang","doi":"10.1002/cbf.70080","DOIUrl":"https://doi.org/10.1002/cbf.70080","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Mechanical ventilation is an effective strategy for managing acute respiratory distress syndrome (ARDS), but it can also exacerbate lung injury, leading to ventilator-induced lung injury (VILI). To investigate the protective role of interleukin-37 (IL-37) in the pathogenesis of VILI, we used two approaches, human IL-37 transgenic (IL37tg) mice and administration of recombinant human IL-37 (rIL37) in wild-type (WT) mice subjected to mechanical ventilation. Lung histopathology was evaluated, inflammatory cytokine levels (IL-1β, IL-6, TNF-α) were measured, and inflammasome activation was assessed by analyzing NLRP3 and Caspase-1 expression. As a result, IL37tg mice exhibited significantly attenuated lung injury compared to WT controls, characterized by improved histological morphology, reduced lung injury scores, and decreased infiltration of macrophages and neutrophils. Similarly, rIL37 administration markedly reduced lung injury and decreased inflammatory cytokine levels. Immunofluorescence analysis revealed colocalization of the alveolar cell marker surfactant protein D (SP-D) and IL-37. Furthermore, IL-37 suppressed NLRP3 inflammasome activation, as evidenced by reduced NLRP3 and Cleaved-Caspase-1 levels in both the IL37tg mouse model and the rIL37 treatment group. These findings suggest that IL-37 effectively protects against VILI by inhibiting inflammation in lung tissues through inhibition of the NLRP3 inflammasome. Therefore, IL-37 may serve as a potential therapeutic target for the prevention and treatment of VILI in the future.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143908957","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":"Irisin Is a Potential Novel Biomarker and Therapeutic Target Against Kidney Diseases","authors":"Xiu Huang,&nbsp;Xiya Ren,&nbsp;Limei Zhao,&nbsp;Yajie Hao,&nbsp;Zhibo Zhao,&nbsp;Fahui Chen,&nbsp;Jinxiu Zhou,&nbsp;Mengqi Bai,&nbsp;Si Chen,&nbsp;Xiaoshuang Zhou","doi":"10.1002/cbf.70075","DOIUrl":"https://doi.org/10.1002/cbf.70075","url":null,"abstract":"<div>\u0000 \u0000 <p>Kidney diseases, characterized by renal dysfunction, are the leading causes of death worldwide. It is crucial to prevent and treat kidney diseases to reduce their associated morbidity and mortality. Moderate physical exercise has been recognized to be advantageous for kidney health. Irisin is an exercise-induced myokine that was identified in 2012. It plays an important role in energy and bone metabolism, oxidative stress reduction, anti-inflammatory processes, cell death inhibition, and cardiovascular protection. However, the relationship between irisin and kidney diseases have not been fully elucidated. This review explores the role of irisin as a biomarker for kidney disease diagnosis and its associated complications, as well as the mechanisms through which it participates in various cell death pathways, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, irisin secretion levels were discussed to provide a basis for kidney disease prevention and treatment avenues, as well as therapeutic guidance for developing new and promising intervention strategies.</p>\u0000 <p><b>Clinical Trial Registration</b>: None.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143896978","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":"P2X7 Receptor Facilitates Cardiomyocyte Autophagy After Myocardial Infarction via Nox4/PERK/ATF4 Signaling Pathway","authors":"Shuhong Zhang,&nbsp;Yingying Bi,&nbsp;Kaili Xiang,&nbsp;Yanhong Tang","doi":"10.1002/cbf.70078","DOIUrl":"https://doi.org/10.1002/cbf.70078","url":null,"abstract":"<div>\u0000 \u0000 <p>Myocardial infarction (MI) represents a critical cardiovascular emergency, standing as a leading cause of global mortality. ATP, a typical damage-associated molecular pattern, is stored in cells at high concentrations. Upon cellular injury, hypoxia, or necrosis, substantial quantities of ATP efflux into the extracellular space, activating P2X₇ receptors, thereby initiating multiple signaling cascades. In vivo studies demonstrated coordinated upregulation of P2X₇ and autophagy-related proteins in the infarcted border zone. Transcriptome sequencing revealed Nox4 overexpression in the myocardial tissue post-infarction; furthermore, administration of the P2X₇ receptor antagonist A740003 effectively reduced both autophagy-related protein levels and Nox4 expression. In vitro experiments indicated that hypoxia induced upregulation of Nox4, p-PERK/PERK, ATF4, Beclin-1, and ATG5 in cardiomyocytes, A740003 could inhibit the expression of these proteins, while overexpression of Nox4 counteracted this effect. Collectively, our findings indicated that the P2X₇ receptor expression was elevated in the infarcted border zone following MI and implicated its role in excessive autophagy induced by hypoxia in cardiomyocytes—at least partially through the Nox4/PERK/ATF4 pathway, thereby exacerbating myocardial injury following MI.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879809","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":"Actin Gamma Smooth Muscle 2 Promotes Epithelial Ovarian Cancer Cell Proliferation via the AKT1/NF-κB Signaling Pathway","authors":"Yinjue Yu,&nbsp;Jiangxia Li,&nbsp;Xiaohang Wang,&nbsp;Xiaoxiao Li,&nbsp;Cuiting Lyu,&nbsp;Lina Yang,&nbsp;Yongrui Bai","doi":"10.1002/cbf.70077","DOIUrl":"https://doi.org/10.1002/cbf.70077","url":null,"abstract":"<div>\u0000 \u0000 <p>Epithelial ovarian cancer (EOC) is associated with high mortality rates worldwide and is characterized as the most lethal gynecological cancer. The study aimed to investigate the functional role and underlying molecular mechanism of actin gamma smooth muscle 2 (<i>ACTG2</i>) in the progression of EOC. Data mining from The Cancer Genome Atlas (TCGA) databases showed the expression of <i>ACTG2</i> was significantly upregulated in EOC and negatively associated with longer overall survival and better prognosis of patients. By using of gain-of-function and loss-of-function experiments in vitro and in vivo, we found that ACTG2 promoted EOC cell proliferation and suppressed cell apoptosis. Mechanistic study revealed that ACTG2 regulates EOC cell proliferation by activating the AKT serine/threonine kinase 1 (AKT1)/nuclear factor-κB (NF-κB) signaling pathway. Importantly, p65 plays a crucial role in this newly identified regulatory mechanism. Our findings demonstrate that ACTG2 may play an oncogenic role in EOC, suggesting its potential as a therapeutic target.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143880005","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":"Cross-Organ Proteome Analysis Reveals Changes in Protein Expression Related With Glucose and Amino Acid Metabolism in Muscles and Hearts of Torpid Mice","authors":"Hirotaka Miyamoto,&nbsp;Shingo Ito,&nbsp;Seiryo Ogata,&nbsp;Ryoko Shimojima,&nbsp;Keiko Sato,&nbsp;Tomoko Kadowaki,&nbsp;Ayako Tokunaga,&nbsp;Kayoko Sato,&nbsp;Yukinobu Kodama,&nbsp;Mihoko N. Nakashima,&nbsp;Koyo Nishida,&nbsp;Mikiro Nakashima,&nbsp;Sumio Ohtsuki,&nbsp;Kaname Ohyama","doi":"10.1002/cbf.70076","DOIUrl":"https://doi.org/10.1002/cbf.70076","url":null,"abstract":"<div>\u0000 \u0000 <p>Mammals undergoing hibernation or torpor can reduce their metabolic rate. However, the mechanisms of hypometabolism in hibernating animals remain unclear. Analysis of hibernation mechanisms, taking into account commonalities and differences among organs, is essential for a comprehensive understanding of this reduction in physiological activity. Therefore, we investigated and compared changes in protein expression in the hearts and skeletal muscles of torpid mice using quantitative proteomics. Most of the 108 proteins commonly decreased in both tissues were related to translation, and the decrease in protein expression under torpid conditions was greater in muscle than in the heart. Furthermore, glycolysis related to proteins and pyruvate dehydrogenase expression was significantly decreased only in skeletal muscle. In contrast, only three proteins had significantly increased expression in the heart and muscles, with pyruvate dehydrogenase kinase 4 being the most increased. These results suggested that glucose consumption was reduced under torpid conditions. Our results suggest that the heart and muscles respond to low nutritional levels during torpor by reducing glucose and amino acid consumption to preserve energy. Moreover, this adaptation occurs more strongly in skeletal muscle than in the heart.</p>\u0000 </div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852842","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":"Dehydrodiisoeugenol Alleviates Sodium Palmitate-Induced Mitochondrial Dysfunction and Activates Autophagy in VSMCs via the SIRT1/Nrf2 Axis","authors":"Zhiyun Shu,&nbsp;Wenqing Zhang,&nbsp;Mengze Sun,&nbsp;Zixu Huyan,&nbsp;Shishun Xie,&nbsp;Hongyuan Cheng,&nbsp;Xiangjun Li","doi":"10.1002/cbf.70074","DOIUrl":"https://doi.org/10.1002/cbf.70074","url":null,"abstract":"<div>\u0000 \u0000 <p>A high-fat model utilizing sodium palmitate (PA) to inhibit vascular smooth muscle cells (VSMCs) was established to evaluate to evaluate the effects of Dehydrodiisoeugenol (Deh) treatment. Proliferative viability was assessed using the CCK8 and EdU assays, while cell migration and autophagy were analyzed via wound healing and Transwell assays, well as the MDC assay. Oxidative stress was measured through reactive oxygen species staining, and superoxide dismutase (SOD) activity was assessed spectrophotometrically. The malondialdehyde (MDA) content was determined using a colorimetric assay. Mitochondrial function was evaluated through membrane potential analysis, and apoptosis was detected using flow cytometry. Bioinformatics and molecular docking studies identified key targets of Deh in treating atherosclerosis (AS), exploring its role in activating autophagy and inhibiting apoptosis through modulation of SIRT1. The results of this study demonstrated that PA significantly inhibited autophagy in VSMCs, suppressed cell proliferation and migration, and promoted oxidative stress, mitochondrial dysfunction, and apoptosis. In contrast, treatment with Deh significantly ameliorated the PA-induced functional impairment of VSMCs. Furthermore, bioinformatics and molecular docking revealed a strong interaction between Deh and SIRT1, suggesting that SIRT1 may serve as a direct therapeutic target for treating AS. The results of the rescue experiments confirmed the relationship between Deh and SIRT1. Compared to Deh administration alone, the combination of Deh with SIRT1 overexpression (OE) further enhanced the proliferation, migration and autophagy of VSMCs while inhibiting oxidative stress, mitochondrial dysfunction, and apoptosis. Additionally, the effects of Deh were reversed by small interfering RNA targeting SIRT1 (si-SIRT1). The Western blot results indicated that Deh could regulate the expression of both SIRT1 and Nrf2, suggesting that the SIRT1/Nrf2 pathway may be involved in the Deh's signaling mechanism. Deh activate autophagy inhibited by PA in VSMCs and mitigates PA-induced mitochondrial dysfunction and apoptosis in these cells through the SIRT1/Nrf2 signaling axis.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831277","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}