International Journal of Biochemistry & Cell Biology最新文献

{"title":"Identify key genes and biological processes participated in obesity-related cancer based on studying 12 cancers","authors":"Lijuan Zhu ,&nbsp;Cuicui Zhao","doi":"10.1016/j.biocel.2025.106764","DOIUrl":"10.1016/j.biocel.2025.106764","url":null,"abstract":"<div><div>Obesity significantly increases the risk of various diseases, particularly cancers, which present a serious threat to public health. Therefore, identifying cancers related to obesity and exploring their pathological pathways and key genes are highly significant for the prevention and treatment of these cancers. In this study, we propose the obesity and cancer edge connectivity based on expanded modular disease genes and expanded modular networks (OCEC_eDMN) algorithm, which based on the disease-related genes, Biological Process (BP) genes, and Protein-Potein Interaction (PPI) network. The algorithm utilizes Random Walk with Restart (RWR) to expand BP genes and disease genes to generate the expanded modular networks (eMNs) and disease genes (eMDs). Finally, this algorithm calculates the average interaction number between eMDs on eMNs. We utilize OCEC_eDMN to predict the ranking of 12 cancers related to obesity/morbid obesity and obtain an AUC of 0.93/0.84. Additionally, OCEC_eDMN reveals the significant BPs associated with obesity-cancer connections. For instance, \"gluconeogenesis\" plays a critical role in the connections between obesity and cancers. Through key driver analysis (KDA) on eMDs, we identify the key connectors in obesity-cancer connections. Genes such as GRB2 are instrumental in linking morbid obesity to colorectal cancer in the eMNs of “response to molecule of bacterial origin”. The significant eMNs and key genes provide valuable references for the prevention and treatment of obesity-related cancers and carry important theoretical implications.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"182 ","pages":"Article 106764"},"PeriodicalIF":3.4,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537849","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":"SIRT2 inhibition attenuates myofibroblast transition through autophagy-mediated ciliogenesis in renal epithelial cells","authors":"Juyoung Son ,&nbsp;Jaejung Park ,&nbsp;Joo-Won Jeong ,&nbsp;Seung Hyeun Lee ,&nbsp;Ja-Eun Kim","doi":"10.1016/j.biocel.2025.106754","DOIUrl":"10.1016/j.biocel.2025.106754","url":null,"abstract":"<div><div>Myofibroblast transition plays a crucial role in both fibrotic diseases and wound healing. Although SIRT2 regulates fibrosis, its mechanisms of action remain poorly understood. This study aimed to investigate the effects of SIRT2 inhibition on myofibroblast transition in human renal cells under quiescent conditions. HK-2 kidney proximal tubular epithelial cells were starved of serum, resulting in the formation of primary cilia. Transforming growth factor-β (TGF-β) stimulation reduced both the number of ciliated cells and ciliary length. The ciliary defects resulted from a failure in autophagy termination, leading to the accumulation of OFD1, a negative regulator of ciliogenesis, at centriolar satellites. This phenomenon was correlated with the upregulation of fibrosis-related proteins. To elucidate the role of SIRT2 in the autophagy−ciliogenesis−fibrosis axis, cells were treated with AGK2, a specific inhibitor of SIRT2. AGK2 treatment promoted the formation of both autophagosomes and autolysosomes and facilitated OFD1 degradation at the centriolar satellites, resulting in the lengthening of primary cilia. Restoration of primary cilia by AGK2 was associated with the suppression of myofibroblast transition. In conclusion, SIRT2 inhibition attenuates TGF-β-induced fibrosis by promoting autophagy-mediated ciliogenesis. This study highlights SIRT2 as a potential therapeutic target for fibrotic diseases.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"181 ","pages":"Article 106754"},"PeriodicalIF":3.4,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484267","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":"Enhancement of wound healing in diabetic mice by topical use of a peptide-ionic liquid conjugate","authors":"Ana Gomes ,&nbsp;Ermelindo C. Leal ,&nbsp;Jessica Da Silva ,&nbsp;Inês Teixeira ,&nbsp;Ricardo Ferraz ,&nbsp;Daniela Calheiros ,&nbsp;Teresa Gonçalves ,&nbsp;Eugénia Carvalho ,&nbsp;Paula Gomes","doi":"10.1016/j.biocel.2025.106753","DOIUrl":"10.1016/j.biocel.2025.106753","url":null,"abstract":"<div><div>Diabetic foot ulcers (DFU) are one of the most devastating complications of diabetes, with high impact on patient’s quality of life. In worst scenarios, DFU can lead to severe amputation or even death. DFUs are an easy target for microbial pathogens and their effective healing is hampered by the galloping increase of microbial resistance to antibiotics, including from the most prevalent pathogens in DFU, <em>e.g. Staphylococcus aureus</em>. As such, available antibiotics show poor efficacy in the treatment of DFU, leading to a chronic condition that is exacerbated by poor healing rates due to the persistent inflammation, poor oxygenation and low angiogenesis, leading to high risk of ischemia, among other conditions that typically affect patients with diabetes. Our group has recently designed new peptide-based strategies towards the topical treatment of DFU, whereby peptide-ionic liquid conjugates emerged as highly promising agents. One of the best such conjugates, C₁₆-Im-PP4, results from coupling an imidazolium-based ionic liquid with intrinsic antimicrobial activity to the <em>N</em>-terminus of a collagen boosting peptide used in cosmetics, the pentapeptide-4. C₁₆-Im-PP4 showed excellent <em>in vitro</em> properties, namely, wide-spectrum antimicrobial action and collagen-boosting effect on human dermal fibroblasts, prompting the <em>in vivo</em> study here reported. The peptide-ionic liquid conjugate was applied topically on wounds of mice with diabetes. The results show multitargeted actions, at a dose of 1 µg/wound including: i) anti-inflammatory; ii) antioxidant; iii) pro-collagenic; vi) pro-angiogenic; v) antimicrobial; and vi) improved wound maturation effects. Altogether, these results identify this technology as a novel topical treatment for DFU.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"180 ","pages":"Article 106753"},"PeriodicalIF":3.4,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419123","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":"Expression analysis of molecular chaperones associated with disaggregation complex in rotenone-induced Parkinsonian rat model","authors":"Tanu ,&nbsp;Minal Chaturvedi ,&nbsp;Siraj Fatima ,&nbsp;Smriti Singh Yadav ,&nbsp;Prabeen Kumar Padhy ,&nbsp;Saurabh Tiwari ,&nbsp;Kavita Seth ,&nbsp;Rajnish K. Chaturvedi ,&nbsp;Smriti Priya","doi":"10.1016/j.biocel.2025.106752","DOIUrl":"10.1016/j.biocel.2025.106752","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the aberrant aggregation and phosphorylation (ser129) of α-synuclein (α-syn, a presynaptic protein) which leads to the formation of pathogenic Lewy bodies. A critical factor in the pathogenesis of PD is the disruption of the cellular protein quality control system, where molecular chaperones and their co-chaperones are integral for mitigating proteotoxic stress. Although the role of molecular chaperones in PD and other protein aggregation diseases has been extensively investigated, the in vivo investigation of disaggregation chaperones, including HSP70, HSP105, and co-chaperone DNAJBs, remains relatively limited. The present study aims to elucidate the expression dynamics of the disaggregation molecular chaperones within the substantia nigra pars compacta of the rotenone-induced Parkinsonian rat model and its association with α-syn aggregation. The rotenone-treated rats exhibited significant behavioural symptoms, α-syn aggregation and degeneration of dopaminergic neurons, confirming the development of Parkinsonism. Significant upregulation of α-syn expression/phosphorylation and co-localization in TH+ve neurons in the SNpc of treated rats was observed. Further, the gene and protein analysis of HSP70, DNAJB6, and HSP105 were found to be upregulated and TH+ve neurons showed their co-localization with p-α-syn^ser129 expression. The total proteomic analysis of SNpc correlated the altered cellular processes with cellular homeostasis imbalance. The observations of the present study provide an in vivo analysis of disaggregation-associated molecular chaperones in Parkinsonian or α-syn related conditions. The study can be helpful for further manipulation in the expression or activity of disaggregation-related chaperones for advanced therapeutic strategies and mechanistic studies in protein aggregation-associated diseases.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"181 ","pages":"Article 106752"},"PeriodicalIF":3.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426554","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":"Identification of a liver fibrosis and disease progression-related transcriptome signature in non-alcoholic fatty liver disease","authors":"Li-Xin Pan ,&nbsp;Wei Tian ,&nbsp;Zhi-Hao Huang ,&nbsp;Jian-Rong Li ,&nbsp;Jia-Yong Su ,&nbsp;Qiu-Yan Wang ,&nbsp;Xiao-Hui Fan ,&nbsp;Jian-Hong Zhong","doi":"10.1016/j.biocel.2025.106751","DOIUrl":"10.1016/j.biocel.2025.106751","url":null,"abstract":"<div><div>Non-alcoholic fatty liver disease (NAFLD)-related liver fibrosis is closely associated with long-term outcomes of patients. This study aimed to establish a transcriptome signature to distinguish NAFLD patients with mild or advanced fibrosis and to monitor disease progression. Using least absolute shrinkage selection operator regression, we identified a signature of 11 hub genes by performing differential gene expression analysis in six bulk transcriptome profiles in the Gene Expression Omnibus database from liver fibrosis patients with different etiologies. Patients with NAFLD were classified using the 11-hub gene signature. Integrated analysis of signaling pathway enrichment, gene set enrichment, nearest template prediction, infiltration by hepatic stellate cells (HSCs) and pseudotime trajectories was performed on three bulk and one single-cell transcriptomes from NAFLD patients. Molecular features were compared between high-risk and low-risk groups, and associations were explored between hub gene signature expression and activation of HSCs. It was found that the high-risk group was characterized by advanced fibrosis stage, elevated risk for hepatocellular carcinoma, more significant infiltration by activated HSCs, as well as enrichment in signaling pathways related to fibrogenesis and NAFLD progression. Moreover, the 11-hub gene signature at the single-cell transcriptome level correlated with HSCs activation. <em>In vitro</em> experiments were conducted to evaluate the expression levels of hub genes, and <em>IL6</em> was found to be up-regulated in activated LX-2 cells showing lipid accumulation. Our findings suggest that the 11-hub gene signature can help identify fibrosis stage in patients with NAFLD and detect disease progression. We also suggest that the role of <em>IL6</em> in HSC activation deserves more investigation in the context of NAFLD.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"180 ","pages":"Article 106751"},"PeriodicalIF":3.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257199","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":"5'tiRNA-33-CysACA-1 promotes septic cardiomyopathy by targeting PGC-1α-mediated mitochondrial biogenesis","authors":"Ludong Yuan ,&nbsp;Jing Li ,&nbsp;Leijing Yin ,&nbsp;Xiaofang Lin ,&nbsp;Dan Ni ,&nbsp;Chuanhuan Deng ,&nbsp;Pengfei Liang ,&nbsp;Bimei Jiang","doi":"10.1016/j.biocel.2024.106714","DOIUrl":"10.1016/j.biocel.2024.106714","url":null,"abstract":"<div><h3>Background</h3><div>We revealed for the first time that the expression of 158 tRNA-derived small RNAs (tsRNAs) was altered in septic cardiomyopathy (SCM) by microarray analysis, and we selected 5'tiRNA-33-CysACA-1, which was the most significantly up-regulated, as a representative to explore the roles and mechanisms of tsRNAs in SCM.</div></div><div><h3>Methods</h3><div>We constructed a sepsis model by cecum ligation and puncture (CLP) in mice and detected the expression of 5'tiRNA-33-CysACA-1 using quantitative real-time PCR (qRT-PCR). The supernatant generated after LPS stimulation of macrophages was used as the conditional medium (CM) to stimulate H9C2 and established the injured cell model. CCK-8 and LDH release assays were used to detect cell viability and cell death. Mitochondrial membrane potential (MMP), ATP production, ROS production, and Mitotracker Red mitochondrial morphology were assayed to assess mitochondrial function. Expression of mRNA for molecules related to the mitochondrial quality control system was verified by qRT-PCR. The mechanism by which 5'tiRNA-33-CysACA-1 regulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) expression was examined by western blot, mRNA stability analysis, and rescue experiments.</div></div><div><h3>Results</h3><div>Expression of 5'tiRNA-33-CysACA-1 was elevated in cardiac tissue and H9C2 cells during septic myocardial injury. Stimulation of the CM resulted in cardiomyocyte injury and impaired mitochondrial function. Transfection of 5'tiRNA-33-CysACA-1 mimic in CM further downregulated PGC-1α expression, inhibited mitochondrial biogenesis thereby impairing mitochondrial function and leading to decreased cardiomyocyte activity and increased cell death. In contrast, transfection of the inhibitor ameliorated the above biological processes. In addition, mRNA stability assay and bioinformatics analysis showed that 5'tiRNA-33-CysACA-1 led to a decrease in the stability of PGC-1α mRNA, which in turn downregulated the expression of PGC-1α and promoted the development of SCM.</div></div><div><h3>Conclusions</h3><div>5'tiRNA-33-CysACA-1 expression is upregulated in SCM and inhibits mitochondrial biogenesis by targeting PGC-1α and decreasing the stability of PGC-1α mRNA, leading to mitochondrial dysfunction and promoting the development of SCM.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106714"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781714","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":"Multi-omics analysis of transcriptome and proteome reveals that BAZ1A and BAZ2A have common and individual regulatory roles in hepatocellular carcinoma","authors":"Yan Liu ,&nbsp;Fenglin Dong ,&nbsp;Shuqing Wang ,&nbsp;Jinghua Wu ,&nbsp;Liming Zhou ,&nbsp;Wei Fang","doi":"10.1016/j.biocel.2024.106730","DOIUrl":"10.1016/j.biocel.2024.106730","url":null,"abstract":"<div><div>This study employs an integrative multi-omics approach to elucidate the complex regulatory roles of BAZ1A and BAZ2A, subunits of the ISWI chromatin remodeling complexes, in hepatocellular carcinoma (HCC). Utilizing siRNA-mediated knockdown, combined with high-throughput RNA sequencing and mass spectrometry, the researchers reveal distinct and overlapping functions of BAZ1A and BAZ2A in both transcriptional and proteomic regulation. The findings indicate that BAZ1A is primarily involved in ribosomal biogenesis and nucleolar function, while BAZ2A exerts significant influence on cell cycle progression and DNA repair mechanisms. Through a comprehensive analysis of the transcriptome and proteome following gene knockdown, the study highlights the intricate interplay between these two subunits, which contributes to the pathogenesis of HCC. This integrated approach not only uncovers their differential impact on gene expression and protein abundance but also reveals their involvement in alternative splicing events. Additionally, potential downstream targets and associated signaling pathways are identified, providing valuable insights into the molecular mechanisms underlying HCC development. The distinct roles of BAZ1A and BAZ2A in various cellular processes, along with their differential effects on gene and protein regulation, position them as promising therapeutic targets. These results offer new perspectives for understanding the molecular basis of HCC and suggest potential avenues for targeted therapies.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106730"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143155572","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":"Corrigendum to “Dimerization of ZIP promotes its transcriptional repressive function and biological activity” [Int. J. Biochem. Cell Biol. 44 (2012) 886–895]","authors":"Bin Gui ,&nbsp;Xiao Han ,&nbsp;Yu Zhang ,&nbsp;Jing Liang ,&nbsp;Dandan Wang ,&nbsp;Chenghao Xuan ,&nbsp;Zhipeng Yu ,&nbsp;Yongfeng Shang","doi":"10.1016/j.biocel.2024.106715","DOIUrl":"10.1016/j.biocel.2024.106715","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106715"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796476","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":"Influence of the ERK/CHGB pathway in breast cancer progression under chronic stress","authors":"Yue Wang ,&nbsp;Xi Hou ,&nbsp;Zijing Wu ,&nbsp;Junyu Ren ,&nbsp;Yanfang Zhao","doi":"10.1016/j.biocel.2024.106733","DOIUrl":"10.1016/j.biocel.2024.106733","url":null,"abstract":"<div><h3>Background</h3><div>Breast cancer is one of the most common malignancies among women, and its development involves a variety of complex molecular mechanisms. Extracellular signal-regulated kinase (ERK) and Chromogranin B (CHGB) are known to play key roles in various cancers. This study aims to explore the impact of the ERK/CHGB pathway in a chronic stress environment simulated by salbutamol on the development of breast cancer.</div></div><div><h3>Methods</h3><div>This study utilized female BALB/c mice to establish a breast cancer model, dividing them into control, salbutamol-treated, and salbutamol-inhibitor-treated groups. Cell culture, immunohistochemistry, Western Blot, real-time fluorescent quantitative PCR, and Transwell migration assays were employed to assess the effects of salbutamol and the ERK/CHGB pathway.</div></div><div><h3>Results</h3><div>Salbutamol treatment significantly enhanced the proliferation, migration, and invasiveness of breast cancer cells, associated with the activation of the ERK pathway and the inhibition of CHGB. The salbutamol-inhibitor-treated group exhibited a marked suppression of these effects. Additionally, the interaction of the ERK/CHGB pathway in an extracellular stress environment provided advantages for the survival and proliferation of breast cancer cells.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that a chronic stress environment simulated by salbutamol can promote malignant behaviors in breast cancer cells through the ERK/CHGB pathway. These findings offer new molecular targets for breast cancer treatment and highlight the potential importance of managing chronic stress and blocking specific molecular pathways in cancer therapy.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106733"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933445","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":"Corrigendum to “ROCK inhibition reduces the sensitivity of mutant p53 glioblastoma to genotoxic stress through a Rac1- driven ROS production” [Int. J. Biochem. Mol. Bio. 164 (2023) 106474–106484]","authors":"Yuli Thamires Magalhaes,&nbsp;Fabio Luis Forti","doi":"10.1016/j.biocel.2024.106732","DOIUrl":"10.1016/j.biocel.2024.106732","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106732"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142958170","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}