Archives of biochemistry and biophysics最新文献

{"title":"Predictive value of LncRNA LINC00667 in the development and prognosis of papillary thyroid carcinoma and its possible regulation of cellular processes via miR-34c-5p","authors":"Qinghua Zhang ,&nbsp;Zhao Liu ,&nbsp;Zhiyong Li ,&nbsp;Xiancun Hou ,&nbsp;Changli Ouyang","doi":"10.1016/j.abb.2025.110683","DOIUrl":"10.1016/j.abb.2025.110683","url":null,"abstract":"<div><h3>Background</h3><div>As a major type of endocrine malignancy, thyroid cancer (THCA) has a relatively high occurrence rate around the world. However, the underlying mechanism through which LINC00667 acts in papillary thyroid carcinoma (PTC) remains unelucidated.</div></div><div><h3>Methods</h3><div>A total of 120 PTC patients were enrolled. The expression of LINC00667 was analyzed using reverse transcription-quantitative polymerase chain reaction. To evaluate the clinical significance of LINC00667, chi-square analysis was performed, a Kaplan-Meier survival curve was generated, and multivariate Cox analysis was conducted to determine its association with the clinical-pathological characteristics and prognostic outcomes of PTC. Cell Counting Kit-8 and Transwell assays evaluated changes in cellular processes. A dual luciferase reporter assay and RNA Immunoprecipitation were employed to analyze the binding relationship between LINC00667 and miR-34c-5p.</div></div><div><h3>Results</h3><div>LINC00667 exhibited significant up-regulation in PTC tissues, with elevated expression levels associated with tumor malignancy. Increased LINC00667 expression was a marker of unfavorable prognostic outcomes and functioned as an independent risk indicator for PTC. Knockdown of LINC00667 expression inhibited the proliferation, migration capability, and invasive properties of PTC cells. Furthermore, LINC00667 was identified to exert a negative regulatory effect on miR-34c-5p, and the silencing of miR-34c-5p weakened the inhibitory impacts induced by LINC00667 depletion on the malignant behaviors of PTC cells.</div></div><div><h3>Conclusions</h3><div>Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110683"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145666861","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 role of miR-491-3p in early diagnosis and prognosis evaluation of acute myocardial infarction","authors":"Tai Dou ,&nbsp;Lijie Qin ,&nbsp;Peirong Zhang,&nbsp;Lijun Xu,&nbsp;Yanwei Cheng,&nbsp;Peng Wang","doi":"10.1016/j.abb.2025.110691","DOIUrl":"10.1016/j.abb.2025.110691","url":null,"abstract":"<div><h3>Aims</h3><div>To investigate the expression characteristics, clinical implications, and underlying mechanisms of miR-491-3p in patients with acute myocardial infarction (AMI).</div></div><div><h3>Methods</h3><div>Serum samples were collected from patients with AMI and healthy controls. miR-491-3p expression was measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic (ROC) curves evaluated its diagnostic accuracy for AMI. Correlations between miR-491-3p levels and myocardial injury markers or inflammatory factors were analyzed. A one-year follow-up assessed its predictive value for major adverse cardiovascular events (MACE). A hypoxia/reoxygenation (H/R) model of human AC16 cardiomyocytes was established to explore the mechanism of miR-491-3p in H/R-induced injury via targeting aquaporin 9 (AQP9).</div></div><div><h3>Results</h3><div>Serum miR-491-3p was significantly downregulated in AMI patients, with an AUC of 0.893 for AMI diagnosis (sensitivity 83 %, specificity 79.5 %). Levels were negatively correlated with myocardial injury markers and inflammatory factors. AMI patients with low miR-491-3p expression had a higher incidence of MACE, and low expression was identified as a risk factor. In the H/R model, miR-491-3p was downregulated. Overexpression of miR-491-3p improved cell proliferation, reduced apoptosis, and decreased inflammatory factors by targeting and inhibiting AQP9.</div></div><div><h3>Conclusions</h3><div>miR-491-3p may be involved in the pathological process of AMI by targeting and regulating AQP9. This makes it a promising candidate as both a diagnostic and prognostic marker for AMI, as well as a potential therapeutic target.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110691"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145686944","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":"Kinetic investigation on d-amino acid containing peptides and carboxypeptidase Y","authors":"Joshua I. Putman,&nbsp;Arzoo Patel,&nbsp;Maria Olds,&nbsp;Alaa Aziz,&nbsp;Haritha Asokan-Sheeja,&nbsp;He Dong,&nbsp;Kayunta L. Johnson-Winters,&nbsp;Daniel W. Armstrong","doi":"10.1016/j.abb.2025.110699","DOIUrl":"10.1016/j.abb.2025.110699","url":null,"abstract":"<div><div>Carboxypeptidases catalyze the hydrolysis of the peptide bond of C terminal amino acid residues. Carboxypeptidase Y can hydrolyze all 20 naturally-occurring amino acids at varying rates under optimal conditions. Previous data suggests that carboxypeptidase Y has more difficulty hydrolyzing <span>d</span>-amino acids from the C terminus of peptides than <span>l</span>-amino acids. This enzyme was used for amino acid sequence determination prior to modern proteomics. However, most modern proteomic methods assume that all peptides are comprised of <span>l<em>-</em></span>amino acids and do not distinguish L<span>-</span>from <span>d<em>-</em></span>amino acids within the peptide sequence. Most existing methods that allow for chiral differentiation require synthetic standards or incur racemization. Steady-state kinetic analysis was performed to elucidate differences in hydrolytic rates between peptides composed solely of <span>l</span>-amino acids at the carboxy-terminal and those incorporating <span>d</span>-amino acids. Our data suggests that the <span>l<em>-</em></span>amino acid exclusive peptides are hydrolyzed at a rate two-to-five orders of magnitude higher than <span>d</span>-amino acid containing peptides. Such differences are necessary to completely digest and eliminate <span>l<em>-</em></span>amino acid exclusive peptides while leaving the carboxy-terminal <span>d<em>-</em></span>amino acid peptides intact. The <span>d<em>-</em></span>amino acid containing peptides can then be preconcentrated to enhance detection limits to facilitate scouting for the desired <span>d<em>-</em></span>amino acid containing peptides. Interestingly, the peptide epimers bind equally well to carboxypeptidase Y on a low μM level, indicating high substrate affinity.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110699"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145740718","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":"Apelin-13 ameliorates myocardial ischemia/reperfusion injury by modulating macrophage polarization","authors":"Hui Jia ,&nbsp;Qiyue Zhao ,&nbsp;Jing Yuan ,&nbsp;Xin Wang ,&nbsp;Hua Chen ,&nbsp;Jinghui Dong ,&nbsp;Chunhua Zhu ,&nbsp;Leonid N. Maslov ,&nbsp;Natalia V. Naryzhnaya ,&nbsp;Yue Guan ,&nbsp;Huijie Ma ,&nbsp;Zan Guo","doi":"10.1016/j.abb.2025.110710","DOIUrl":"10.1016/j.abb.2025.110710","url":null,"abstract":"<div><div>Macrophage polarization plays a crucial role in myocardial ischemia/reperfusion (I/R) injury. Although Apelin-13 is known for its anti-inflammatory effects, its impact on macrophage polarization during myocardial I/R injury remains unclear. This study aimed to investigate the effects of Apelin-13 on macrophage polarization and cardiac function in a rat I/R model and H9c2 cells in vitro. I/R injury was induced by ligating the left anterior descending coronary artery with reperfusion times of 2 h and 7 days. H9c2 cells and peritoneal macrophages were cultured in vitro. We show that Apelin-13 significantly improves cardiac function and reduces infarct size in a rat I/R model, as evidenced by improved hemodynamic and echocardiographic parameters. Apelin-13 treatment decreased myocardial apoptosis by modulating the Bcl-2/Bax ratio and shifted macrophage polarization from the pro-inflammatory M1 phenotype to the reparative M2 phenotype in vivo. In vitro, Apelin-13 suppressed LPS-induced pro-inflammatory cytokine production and promoted M2 markers in rat peritoneal macrophages. Furthermore, conditioned medium from Apelin-13-treated macrophages enhanced H9c2 cell survival following oxygen-glucose deprivation/reoxygenation. These findings suggest Apelin-13 as a promising therapeutic strategy for myocardial I/R injury by modulating macrophage polarization and reducing cardiomyocyte apoptosis.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110710"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809257","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":"mmu_circ_0000684/hsa_circ_0067098 mediates renal tubular epithelial cells apoptosis to ischemia-reperfusion-induced acute kidney injury by targeting the mmu_miR_671-5p/ARID3B axis","authors":"Ben Yang ,&nbsp;Qiang Zheng ,&nbsp;Yan Pu ,&nbsp;Yingying Hu ,&nbsp;Dongshan Zhang","doi":"10.1016/j.abb.2025.110679","DOIUrl":"10.1016/j.abb.2025.110679","url":null,"abstract":"<div><h3>Objective</h3><div>This investigation sought to explore the possible role of mmu_circ_0000684 and its homolog hsa_circ_0067098 in the evolution of ischemia-reperfusion-induced acute kidney injury (AKI), with an emphasis on their viability as therapeutic targets.</div></div><div><h3>Method</h3><div>A model was constructed employing Boston University mouse proximal tubule (BUMPT) cells, human renal tubular epithelial (HK-2) cells, and murine kidney tissue. The mmu_circ_0000684, miR-671-5p, and ARID3B mRNA levels, along with their corresponding protein expression, underwent quantification via real-time quantitative polymerase chain reaction and Western blot. A comprehensive examination of the biological roles and signaling cascade of mmu_circ_0000684 and hsa_circ_0067098 was executed utilizing bioinformatics prediction, luciferase reporter assays, fluorescence in situ hybridization, flow cytometry, hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining.</div></div><div><h3>Results</h3><div>Ischemic stress was observed to induce mmu_circ_0000684 expression. Functionally, mmu_circ_0000684 was implicated in promoting BUMPT cell apoptosis as a consequence of ischemia-reperfusion injury. Mechanistically, mmu_circ_0000684 acted as a molecular sponge for miR-671-5p, thereby facilitating the upregulation of ARID3B, which in turn contributed to apoptosis induction. Moreover, silencing mmu_circ_0000684 markedly mitigated ischemia-triggered AKI via modulation of the miR-671-5p/ARID3B axis. Notably, hsa_circ_0067098, the homolog of mmu_circ_0000684, exhibited an analogous regulatory role in HK-2 cells.</div></div><div><h3>Conclusion</h3><div>The mmu_circ_0000684, hsa_circ_0067098/miR-671-5p/ARID3B signaling cascade emerges as an essential mechanism during ischemic AKI progression. Consequently, hsa_circ_0067098 represents a promising therapeutic candidate for addressing ischemic AKI.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110679"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145647308","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":"RHAU helicase affects testosterone synthesis by regulating the Star 3′ UTR region","authors":"Zhongyu Qin ,&nbsp;Kaixia Li ,&nbsp;Yang Song ,&nbsp;Yuwen Wu ,&nbsp;Haorui Wang ,&nbsp;Xuanjie Li ,&nbsp;Jiayi Huang ,&nbsp;Shuaishuai Shi ,&nbsp;Yiqiang Zhang","doi":"10.1016/j.abb.2025.110690","DOIUrl":"10.1016/j.abb.2025.110690","url":null,"abstract":"<div><div>This study investigates the role and regulatory mechanism of RNA helicase and RNA-binding protein RHAU in testosterone synthesis. Using molecular biology techniques, such as circular dichroism spectroscopy, RNA-protein interaction assays, gene expression analysis, and ELISA functional assays, we explored the interaction between RHAU and the 3′ untranslated region of <em>Star</em> mRNA, and its effect on mRNA stability and translation efficiency. The results show that conditional knockdown of RHAU leads to decreased testosterone levels in mouse blood, reduced translation of steroidogenic acute regulatory protein (STAR), and significantly increased apoptosis of testicular interstitial cells. RHAU specifically binds to the G-quadruplex structure in the 3′ untranslated region of <em>Star</em> mRNA, regulating STAR expression and affecting testosterone synthesis. This study is the first to reveal the critical role of RHAU in testosterone synthesis and post-transcriptional regulation. Moreover, RHAU emerges as a potential therapeutic target for diseases related to testosterone imbalance.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110690"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699350","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 impact of urinary calcium-binding and oxalate-binding proteins on modulation of calcium oxalate renal calculi","authors":"Sudarat Hadpech,&nbsp;Paleerath Peerapen,&nbsp;Visith Thongboonkerd","doi":"10.1016/j.abb.2025.110712","DOIUrl":"10.1016/j.abb.2025.110712","url":null,"abstract":"<div><div>Cumulative data suggest that proteins with modulatory activities on calcium oxalate (CaOx) renal calculi commonly have calcium-binding and/or oxalate-binding domains/motifs. However, the information on calcium-binding proteins (CaBPs) and oxalate-binding proteins (OxBPs) in the urine of healthy individuals and stone formers was not available. Herein, we addressed the impact of urinary CaBPs and OxBPs on CaOx renal calculi. Large proteome datasets from recent/previous quantitative proteomics studies and all known CaOx stone modulatory proteins listed on the StoneMod (<span><span>www.stonemod.org</span><svg><path></path></svg></span>) database were retrieved and analyzed for calcium-binding and/or oxalate-binding domains/motifs. The data showed that %CaBPs decreased, whereas no. of oxalate-binding sites/protein increased in stone formers' urine. Among differentially excreted proteins, %CaBPs tended to reduce, whereas no. of oxalate-binding sites/protein tended to be greater in those with increased levels in stone formers’ urine. Interestingly, known CaOx stone inhibitory proteins tended to have greater %CaBPs and no. of calcium-binding sites/protein, whereas known CaOx promoters had no CaBPs and tended to have greater %OxBPs. Moreover, CaOx crystallization fold-change induced by the known modulators inversely correlated with no. of calcium-binding sites/protein. These data implicate the impact of CaBPs and OxBPs on CaOx renal calculi, i.e., CaBPs tend to inhibit, whereas OxBPs tend to promote CaOx calculi development.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110712"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826585","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":"Nucleotide-dependent structural dynamics and domain motion in Coxiella burnetii EngA GTPases: Insights from molecular dynamics simulation","authors":"K.M. Kavya ,&nbsp;Guruswaroop C ,&nbsp;Upendra N ,&nbsp;Krishnaveni S","doi":"10.1016/j.abb.2025.110693","DOIUrl":"10.1016/j.abb.2025.110693","url":null,"abstract":"<div><div>EngA, a ribosome-associated bacterial GTPase essential for 50S subunit maturation and bacterial growth, lacks a human ortholog, making it an attractive antibacterial target. Its activity is governed by a nucleotide-dependent molecular switch: GTP binding promotes EngA association with the immature 50S subunit and facilitates rRNA processing, whereas GTP hydrolysis to GDP triggers dissociation from the ribosome. Structural studies on <em>Bacillus subtilis</em> EngA revealed that GTP-analog-bound EngA disrupts the GD1-KH interface required for 45S subunit association, while GDP-bound EngA retains these interactions. However, the molecular mechanism by which nucleotides regulate these transitions and whether similar mechanisms exist in other pathogenic species remain unclear. To address this, 1000 ns molecular dynamics simulations of <em>Coxiella burnetii</em> EngA was performed in four nucleotide-bound states: [GDP:GDP], [GDP:GTP-Mg²⁺], [GTP-Mg²⁺:GDP], and [GTP-Mg²⁺:GTP-Mg²⁺]. Analyses of principal components, interaction energies, and distance-angle parameters revealed nucleotide-dependent domain dynamics. In the [GTP-Mg²⁺:GTP-Mg²⁺] state, GD1 and KH domains moved apart, forming an open conformation, while in [GDP:GDP] they approached each other, forming a closed conformation consistent with cryo-EM structures. Community network analysis further showed that GDP binding to GD1 extends connectivity from the nucleotide to SwI, stabilizing SwI-KH interactions and restricting GD1 motion. In contrast, GTP-Mg²⁺ binding disrupts this network, enabling SwI-GD2 interactions that weaken the GD1-KH interface and promote an open conformation. Overall, the results highlight how nucleotide charge-dependent interactions regulate EngA allosteric network and drive its conformational switching mechanism.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110693"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696009","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 “Dihydrocelastrol induces cell death and suppresses angiogenesis through BCR/AP-1/junb signalling in diffuse large B cell lymphoma” [Arch. Biochem. Biophys. 754 (2024) 109929]","authors":"Yue Lai ,&nbsp;Shushan Guo ,&nbsp;Qiongwei Tang ,&nbsp;Gaomei Chang ,&nbsp;Hui Zhang ,&nbsp;Bo Li ,&nbsp;Qilin Feng ,&nbsp;Ke Hu ,&nbsp;Zhijian Xu ,&nbsp;Xuejie Gao ,&nbsp;Qikai Zhang ,&nbsp;Hongfei Yi ,&nbsp;Dongliang Song ,&nbsp;Yifei Zhang ,&nbsp;Yu Peng ,&nbsp;Haiyan Cai ,&nbsp;Weiliang Zhu ,&nbsp;Jumei Shi","doi":"10.1016/j.abb.2025.110652","DOIUrl":"10.1016/j.abb.2025.110652","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"776 ","pages":"Article 110652"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399652","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 \"Folic acid-functionalized and acetyl-terminated dendrimers as nanovectors for co-delivery of sorafenib and 5-fluorouracil\" [Arch. Biochem. Biophys. 762C (2024) 110176].","authors":"Ali Hussein Mezher, Mahboobeh Salehpour, Zohreh Saadati","doi":"10.1016/j.abb.2025.110729","DOIUrl":"10.1016/j.abb.2025.110729","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110729"},"PeriodicalIF":3.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931936","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}