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Thermal Behavior in Relation to Different Bindings of Alumina Based Castables from 20 to 1000℃ 被引量:5
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作者 ZHOU Ningsheng LIU Min ZHANG Sanhua 《China's Refractories》 CAS 2006年第4期3-6,共4页
Thermal behavior and physical properties of castables during curing and drying-out are associated with their binding system. In this work, five alumina based ( Al2O3 〉 87% ) castables with different combinations of... Thermal behavior and physical properties of castables during curing and drying-out are associated with their binding system. In this work, five alumina based ( Al2O3 〉 87% ) castables with different combinations of binding materials, i. e. , ( 1 ) CA cement (CA) + Reactive alumina ( RA ) + H2O ; ( 2 ) high level addi- tion of CA + Microsilica (MS) + H2O ; ( 3 ) low level addition of CA + MS + H2O ; (4) MS + Hydratable alumina + H20 and ( 5 ) MS + Magnesia + H2O, respectively, have been investigated on the flowability and thermal behavior during curing at room temperature, drying at 110% and heating from 200℃ to 1000℃ at an interval of 100℃ , in terms of water addition, vibration flow value, porosity, dehydration, explosion resistance, cold and hot bending strengths. Differences in dehydrating behavior and the mentioned properties have been revealed and correlated to the binding system. 展开更多
关键词 BINDING FLOWABILITY Thermal behavior Alumina based castables
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Computational Analysis for Residue-Specific CDK2-Inhibitor Bindings
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作者 Yun-peng Yang Li-ping He +2 位作者 Jing-xiao Bao Yi-fei Qi John Z. H. Zhang 《Chinese Journal of Chemical Physics》 SCIE CAS CSCD 2019年第1期134-142,I0003,共10页
Cyclin-dependent kinase 2 (CDK2) is a key macromolecule in cell cycle regulation. In cancer cells, CDK2 is often overexpressed and its inhibition is an effective therapy of many cancers including breast carcinomas, le... Cyclin-dependent kinase 2 (CDK2) is a key macromolecule in cell cycle regulation. In cancer cells, CDK2 is often overexpressed and its inhibition is an effective therapy of many cancers including breast carcinomas, leukemia, and lymphomas. Quantitative characterization of the interactions between CDK2 and its inhibitors at atomic level may provide a deep understanding of protein-inhibitor interactions and clues for more effective drug discovery. In this study, we have used the computational alanine scanning approach in combination with an efficient interaction entropy method to study the microscopic mechanism of binding between CDK2 and its 13 inhibitors. The total binding free energy from the method shows a correlation of 0.76?0.83 with the experimental values. The free energy component reveals two binding mode in the 13 complexes, namely van der Waals dominant, and electrostatic dominant. Decomposition of the total energy to per-residue contribution allows us to identify five hydrophobic residues as hot spots during the binding. Residues that are responsible for determining the strength of the binding were also analyzed. 展开更多
关键词 CDK2 MD simulation INHIBITOR Hot-spot residue Binding free energy
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基于网络药理学和分子对接技术的灵芝改善2型糖尿病作用机制 被引量:1
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作者 高德勐 付钰涓 +1 位作者 蒲馨怡 徐广宇 《北华大学学报(自然科学版)》 CAS 2024年第3期339-345,共7页
目的应用网络药理学方法探讨灵芝在改善2型糖尿病(T2DM)中的作用机制。方法通过TCMSP筛选灵芝化学成分,使用SWISS Target Prediction导入主要成分的SMILE name获取单个基因名;结合DisGeNET和GeneCards获取疾病基因;利用Venn数据库筛选... 目的应用网络药理学方法探讨灵芝在改善2型糖尿病(T2DM)中的作用机制。方法通过TCMSP筛选灵芝化学成分,使用SWISS Target Prediction导入主要成分的SMILE name获取单个基因名;结合DisGeNET和GeneCards获取疾病基因;利用Venn数据库筛选出交集靶点;在微生信平台构建活性成分和疾病靶点网络;利用STRING和Cytoscape数据库构建PPI网络;使用DAVID数据库进行GO和KEGG功能富集分析;使用AutoDock数据库进行分子对接。结果灵芝和2型糖尿病的共同靶点有146个;PPI网络包含灵芝和2型糖尿病共同目标有146个节点和2201条“边”;筛选出灵芝5个活性成分及与T2DM相关靶点146个;重要活性成分包括Methyl lucidenate F、环氧灵芝醇A、赤灵芝酸E、赤芝酮A、Methyl lucidenate Q,核心靶点包括PGR、PTPN1、NR3C2等;KEGG主要通路富集于卵母细胞减数分裂、NF-kappa B信号通路、长寿调节途径等;分子对接结果显示,化合物和重要靶位之间具有很强的融合作用。结论本研究进一步发现了灵芝中含有Methyl lucidenate F、环氧灵芝醇A、赤紫芝酸e、赤芝酸A、Methyl lucidenate Q等活性成分,为灵芝治疗2型糖尿病的核心组分,通过控制关键治疗靶点NR3C2和HSD11B2,影响NF-kappaB binding信息通路,从而达到改善2型糖尿病的效果。 展开更多
关键词 2型糖尿病 灵芝 网络药理学 NF-kappaB binding通路 分子对接
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A comparison study on structure-function relationship of polysaccharides obtained from sea buckthorn berries using different methods:antioxidant and bile acid-binding capacity 被引量:5
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作者 Qiaoyun Li Zuman Dou +5 位作者 Qingfei Duan Chun Chen Ruihai Liu Yueming Jiang Bao Yang Xiong Fu 《Food Science and Human Wellness》 SCIE CSCD 2024年第1期494-505,共12页
In this study,the structural characters,antioxidant activities and bile acid-binding ability of sea buckthorn polysaccharides(HRPs)obtained by the commonly used hot water(HRP-W),pressurized hot water(HRP-H),ultrasonic... In this study,the structural characters,antioxidant activities and bile acid-binding ability of sea buckthorn polysaccharides(HRPs)obtained by the commonly used hot water(HRP-W),pressurized hot water(HRP-H),ultrasonic(HRP-U),acid(HRP-C)and alkali(HRP-A)assisted extraction methods were investigated.The results demonstrated that extraction methods had significant effects on extraction yield,monosaccharide composition,molecular weight,particle size,triple-helical structure,and surface morphology of HRPs except for the major linkage bands.Thermogravimetric analysis showed that HRP-U with filamentous reticular microstructure exhibited better thermal stability.The HRP-A with the lowest molecular weight and highest arabinose content possessed the best antioxidant activities.Moreover,the rheological analysis indicated that HRPs with higher galacturonic acid content and molecular weight showed higher viscosity and stronger crosslinking network(HRP-C,HRP-W and HRP-U),which exhibited stronger bile acid binding capacity.The present findings provide scientific evidence in the preparation technology of sea buckthorn polysaccharides with good antioxidant and bile acid binding capacity which are related to the structure affected by the extraction methods. 展开更多
关键词 Sea buckthorn Extraction method STRUCTURE Rheological properties Antioxidant activity Bile acid binding capacity
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Post-transcriptional mechanisms controlling neurogenesis and direct neuronal reprogramming 被引量:1
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作者 Elsa Papadimitriou Dimitra Thomaidou 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期1929-1939,共11页
Neurogenesis is a tightly regulated process in time and space both in the developing embryo and in adult neurogenic niches.A drastic change in the transcriptome and proteome of radial glial cells or neural stem cells ... Neurogenesis is a tightly regulated process in time and space both in the developing embryo and in adult neurogenic niches.A drastic change in the transcriptome and proteome of radial glial cells or neural stem cells towards the neuronal state is achieved due to sophisticated mechanisms of epigenetic,transcriptional,and post-transcriptional regulation.Understanding these neurogenic mechanisms is of major importance,not only for shedding light on very complex and crucial developmental processes,but also for the identification of putative reprogramming factors,that harbor hierarchically central regulatory roles in the course of neurogenesis and bare thus the capacity to drive direct reprogramming towards the neuronal fate.The major transcriptional programs that orchestrate the neurogenic process have been the focus of research for many years and key neurogenic transcription factors,as well as repressor complexes,have been identified and employed in direct reprogramming protocols to convert non-neuronal cells,into functional neurons.The post-transcriptional regulation of gene expression during nervous system development has emerged as another important and intricate regulatory layer,strongly contributing to the complexity of the mechanisms controlling neurogenesis and neuronal function.In particular,recent advances are highlighting the importance of specific RNA binding proteins that control major steps of mRNA life cycle during neurogenesis,such as alternative splicing,polyadenylation,stability,and translation.Apart from the RNA binding proteins,microRNAs,a class of small non-coding RNAs that block the translation of their target mRNAs,have also been shown to play crucial roles in all the stages of the neurogenic process,from neural stem/progenitor cell proliferation,neuronal differentiation and migration,to functional maturation.Here,we provide an overview of the most prominent post-transcriptional mechanisms mediated by RNA binding proteins and microRNAs during the neurogenic process,giving particular emphasis on the interplay of specific RNA binding proteins with neurogenic microRNAs.Taking under consideration that the molecular mechanisms of neurogenesis exert high similarity to the ones driving direct neuronal reprogramming,we also discuss the current advances in in vitro and in vivo direct neuronal reprogramming approaches that have employed microRNAs or RNA binding proteins as reprogramming factors,highlighting the so far known mechanisms of their reprogramming action. 展开更多
关键词 direct neuronal reprogramming in vivo glia-to-neuron conversion microRNAs NEUROGENESIS post-transcriptional regulation RNA binding proteins
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Neuronal conversion from glia to replenish the lost neurons 被引量:1
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作者 Shiyu Liang Jing Zhou +2 位作者 Xiaolin Yu Shuai Lu Ruitian Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1446-1453,共8页
Neuronal injury,aging,and cerebrovascular and neurodegenerative diseases such as cerebral infarction,Alzheimer’s disease,Parkinson’s disease,frontotemporal dementia,amyotrophic lateral sclerosis,and Huntington’s di... Neuronal injury,aging,and cerebrovascular and neurodegenerative diseases such as cerebral infarction,Alzheimer’s disease,Parkinson’s disease,frontotemporal dementia,amyotrophic lateral sclerosis,and Huntington’s disease are characte rized by significant neuronal loss.Unfo rtunately,the neurons of most mammals including humans do not possess the ability to self-regenerate.Replenishment of lost neurons becomes an appealing therapeutic strategy to reve rse the disease phenotype.Transplantation of pluripotent neural stem cells can supplement the missing neurons in the brain,but it carries the risk of causing gene mutation,tumorigenesis,severe inflammation,and obstructive hydrocephalus induced by brain edema.Conversion of neural or non-neural lineage cells into functional neurons is a promising strategy for the diseases involving neuron loss,which may overcome the above-mentioned disadvantages of neural stem cell therapy.Thus far,many strategies to transfo rm astrocytes,fibroblasts,microglia,Muller glia,NG2 cells,and other glial cells to mature and functional neurons,or for the conversion between neuronal subtypes have been developed thro ugh the regulation of transcription factors,polypyrimidine tra ct binding protein 1(PTBP1),and small chemical molecules or are based on a combination of several factors and the location in the central nervous system.However,some recent papers did not obtain expected results,and discrepancies exist.Therefore,in this review,we discuss the history of neuronal transdifferentiation,summarize the strategies for neuronal replenishment and conversion from glia,especially astrocytes,and point out that biosafety,new strategies,and the accurate origin of the truly co nverted neurons in vivo should be focused upon in future studies.It also arises the attention of replenishing the lost neurons from glia by gene therapies such as up-regulation of some transc ription factors or downregulation of PTBP1 or drug interfe rence therapies. 展开更多
关键词 ASTROCYTES neural stem cells neurodegenerative diseases neuron polypyrimidine tract binding protein 1 repair REPROGRAMMING small molecule transcription factor TRANSDIFFERENTIATION
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Computational Simulation of Aptamer-target Binding Mechanisms
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作者 YANG Yuan-Yuan XU Fei WU Xiu-Xiu 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2024年第11期1550-1562,共13页
Aptamers are a type of single-chain oligonucleotide that can combine with a specific target.Due to their simple preparation,easy modification,stable structure and reusability,aptamers have been widely applied as bioch... Aptamers are a type of single-chain oligonucleotide that can combine with a specific target.Due to their simple preparation,easy modification,stable structure and reusability,aptamers have been widely applied as biochemical sensors for medicine,food safety and environmental monitoring.However,there is little research on aptamer-target binding mechanisms,which limits their application and development.Computational simulation has gained much attention for revealing aptamer-target binding mechanisms at the atomic level.This work summarizes the main simulation methods used in the mechanistic analysis of aptamer-target complexes,the characteristics of binding between aptamers and different targets(metal ions,small organic molecules,biomacromolecules,cells,bacteria and viruses),the types of aptamer-target interactions and the factors influencing their strength.It provides a reference for further use of simulations in understanding aptamer-target binding mechanisms. 展开更多
关键词 computational simulation APTAMER TARGET binding mechanism intermolecular forces
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Reliable calculations of nuclear binding energies by the Gaussian process of machine learning
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作者 Zi-Yi Yuan Dong Bai +1 位作者 Zhen Wang Zhong-Zhou Ren 《Nuclear Science and Techniques》 SCIE EI CAS CSCD 2024年第6期130-144,共15页
Reliable calculations of nuclear binding energies are crucial for advancing the research of nuclear physics. Machine learning provides an innovative approach to exploring complex physical problems. In this study, the ... Reliable calculations of nuclear binding energies are crucial for advancing the research of nuclear physics. Machine learning provides an innovative approach to exploring complex physical problems. In this study, the nuclear binding energies are modeled directly using a machine-learning method called the Gaussian process. First, the binding energies for 2238 nuclei with Z > 20 and N > 20 are calculated using the Gaussian process in a physically motivated feature space, yielding an average deviation of 0.046 MeV and a standard deviation of 0.066 MeV. The results show the good learning ability of the Gaussian process in the studies of binding energies. Then, the predictive power of the Gaussian process is studied by calculating the binding energies for 108 nuclei newly included in AME2020. The theoretical results are in good agreement with the experimental data, reflecting the good predictive power of the Gaussian process. Moreover, the α-decay energies for 1169 nuclei with 50 ≤ Z ≤ 110 are derived from the theoretical binding energies calculated using the Gaussian process. The average deviation and the standard deviation are, respectively, 0.047 MeV and 0.070 MeV. Noticeably, the calculated α-decay energies for the two new isotopes ^ (204 )Ac(Huang et al. Phys Lett B 834, 137484(2022)) and ^ (207) Th(Yang et al. Phys Rev C 105, L051302(2022)) agree well with the latest experimental data. These results demonstrate that the Gaussian process is reliable for the calculations of nuclear binding energies. Finally, the α-decay properties of some unknown actinide nuclei are predicted using the Gaussian process. The predicted results can be useful guides for future research on binding energies and α-decay properties. 展开更多
关键词 Nuclear binding energies DECAY Machine learning Gaussian process
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Investigation into IgG/IgE binding capacity and gut microbiota of digestion products derived from glycated ovalbumin
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作者 Jihua Mao Yanhong Shao +2 位作者 Hui Wang Jun Liu Zongcai Tu 《Food Science and Human Wellness》 SCIE CAS CSCD 2024年第6期3633-3641,共9页
Gut microbiota plays an important role in food allergy.The immunoglobulin G(IgG)/immunoglobulin E(IgE)binding capacity and human gut microbiota changes of digestion products derived from glycated ovalbumin(OVA)were in... Gut microbiota plays an important role in food allergy.The immunoglobulin G(IgG)/immunoglobulin E(IgE)binding capacity and human gut microbiota changes of digestion products derived from glycated ovalbumin(OVA)were investigated.Gastrointestinal digestion effectively destroyed the primary structure of glycated OVA,resulting in a significantly higher digestibility than gastric digestion,and more abundant peptides<3 kDa.Moreover,gastric and gastrointestinal digestion products have different fluorescence quenching and red shift of fluorescence peaks,and possess different conformational structures.These changes resulted in a decrease in 28.7%of the IgE binding capacity of gastrointestinal digestion products beyond that of pepsin.Moreover,gastrointestinal digestion products of glycated OVA increased significantly the proportion of Subdoligranulum,Collinsella,and Bifidobacterium.Therefore,gastrointestinal digestion products of glycated OVA altered human intestinal microbiota,reducing the risk of potential allergy. 展开更多
关键词 OVALBUMIN Glycation DIGESTION IgG/IgE binding capacity Gut microbiota
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Analysis of RNA Recognition and Binding Characteristics of OsCPPR1 Protein in Rice
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作者 ZHENG Shaoyan CHEN Junyu +3 位作者 LI Huatian LIU Zhenlan LI Jing ZHUANG Chuxiong 《Rice science》 SCIE CSCD 2024年第2期215-225,I0032-I0035,共15页
Pentatricopeptide repeat(PPR)proteins represent one of the largest protein families in plants and typically localize to organelles like mitochondria and chloroplasts.By contrast,CYTOPLASMLOCALIZED PPR1(OsCPPR1)is a cy... Pentatricopeptide repeat(PPR)proteins represent one of the largest protein families in plants and typically localize to organelles like mitochondria and chloroplasts.By contrast,CYTOPLASMLOCALIZED PPR1(OsCPPR1)is a cytoplasm-localized PPR protein that can degrade OsGOLDENLIKE1(OsGLK1)mRNA in the tapetum of rice anther.However,the mechanism,by which OsCPPR1 recognizes and binds to OsGLK1 transcripts,remains unknown.Through protein structure prediction and macromolecular docking experiments,we observed that distinct PPR motif structures of OsCPPR1 exhibited varying binding efficiencies to OsGLK1 RNA.Moreover,RNA-electrophoretic mobility shift assay experiment demonstrated that the recombinant OsCPPR1 can directly recognize and bind to OsGLK1 mRNA in vitro.This further confirmed that the mutations in the conserved amino acids in each PPR motif resulted in loss of activity,while truncation of OsCPPR1 decreased its binding efficiency.These findings collectively suggest that it may require some co-factors to assist in cleavage,a facet that warrants further exploration in subsequent studies. 展开更多
关键词 OsCPPR1 RNA recognition and binding pentatricopeptide repeat RICE
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Accelerating Factor Xa inhibitor discovery with a de novo drug design pipeline
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作者 Yujing Zhao Qilei Liu +3 位作者 Jian Du Qingwei Meng Liang Sun Lei Zhang 《Chinese Journal of Chemical Engineering》 SCIE EI CAS CSCD 2024年第8期85-94,共10页
Small-molecule drugs are essential for maintaining human health. The objective of this study is to identify a molecule that can inhibit the Factor Xa protein and be easily procured. An optimization-based de novo drug ... Small-molecule drugs are essential for maintaining human health. The objective of this study is to identify a molecule that can inhibit the Factor Xa protein and be easily procured. An optimization-based de novo drug design framework, Drug CAMD, that integrates a deep learning model with a mixed-integer nonlinear programming model is used for designing drug candidates. Within this framework, a virtual chemical library is specifically tailored to inhibit Factor Xa. To further filter and narrow down the lead compounds from the designed compounds, comprehensive approaches involving molecular docking,binding pose metadynamics(BPMD), binding free energy calculations, and enzyme activity inhibition analysis are utilized. To maximize efficiency in terms of time and resources, molecules for in vitro activity testing are initially selected from commercially available portions of customized virtual chemical libraries. In vitro studies assessing inhibitor activities have confirmed that the compound EN300-331859shows potential Factor Xa inhibition, with an IC_(50)value of 34.57 μmol·L^(-1). Through in silico molecular docking and BPMD, the most plausible binding pose for the EN300-331859-Factor Xa complex are identified. The estimated binding free energy values correlate well with the results obtained from biological assays. Consequently, EN300-331859 is identified as a novel and effective sub-micromolar inhibitor of Factor Xa. 展开更多
关键词 Chemical product design Mathematical programming method Deep learning Binding affinity Factor Xa inhibitor
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Characteristics of long-distance mobile mRNAs from shoot to root in grafted plant species
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作者 Mengmeng Fu Zhen Xu +7 位作者 Huaying Ma Yifan Hao Ji Tian Yi Wang Xinzhong Zhang Xuefeng Xu Zhenhai Han Ting Wu 《Horticultural Plant Journal》 SCIE CAS CSCD 2024年第1期25-37,共13页
Thousands of long-distance mobile mRNAs were identified from different grafting systems,based on high-throughput sequencing technology.Moreover,the long-distance delivery of RNAs was proved to involve multiple mechani... Thousands of long-distance mobile mRNAs were identified from different grafting systems,based on high-throughput sequencing technology.Moreover,the long-distance delivery of RNAs was proved to involve multiple mechanisms.Here,we analyzed the homology,motif,and tRNA-like structure(TLS)of long-distance mobile mRNAs identified by RNA-seq as well as the RNA-binding protein(RBP)in nine grafting combinations including Arabidopsis thaliana,Vitis vinifera,Cucumis sativus,Citrullus lanatus,Nicotiana benthamiana,Malus domestica,Pyrus spp.,Glycine max and Phaseolus vulgaris.Although several mRNAs were found to be shared in herbaceous,woody,and related species,the vast majority of long-distance mobile mRNAs were species-specific.Four non-specific movement-related motifs were identified,while the TLS was not necessary for mRNA long distance mobility.In addition,we found that RBPs were conserved among herbaceous and woody plants as well as related species.This paper reports a further in-depth analysis of the endogenous mechanisms by which the species-specific transportable m RNAs were selected by bioinformatics,in order to provide insights for future research on long-distance mobile mRNAs. 展开更多
关键词 Grafting combination Long-distance mobile mRNA TLS RNA binding proteins
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Megestrol acetate plus metformin for fertility-sparing treatment of atypical endometrial hyperplasia and early-stage endometrial adenocarcinoma: a prospective study
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作者 Yuanyuan WANG Tianjiao LAI +4 位作者 Danxia CHU Jing BAI Shuping YAN Haixia QIN Ruixia GUO 《南方医科大学学报》 CAS CSCD 北大核心 2024年第11期2055-2062,共8页
Objective To evaluate the efficacy of medroxyprogesterone acetate(MA)plus metformin as the primary fertility-sparing treatment for atypical endometrial hyperplasia(AEH)and early-stage grade 1 endometrial adenocarcinom... Objective To evaluate the efficacy of medroxyprogesterone acetate(MA)plus metformin as the primary fertility-sparing treatment for atypical endometrial hyperplasia(AEH)and early-stage grade 1 endometrial adenocarcinoma(G1 EAC)and the recurrence rate after treatment.Methods Sixty patients(aged 20-42 years)with AEH and/or grade 1 EAC limited to the endometrium were enrolled prospectively and randomized into two groups(n=30)to receive oral MA treatment at the daily dose of 160 mg(control)or MA plus oral metformin(850 mg,twice a day)for at least 6 months.The treatment could extend to 12 months until a complete response(CR)was achieved,and follow-up hysteroscopy and curettage were performed every 3 months.For all the patients who achieved CR,endometrial expressions of IGFBP-rP1,p-Akt and p-AMPK were detected immunohistochemically.Results A total of 58 patients completed the treatment.After 9 months of treatment,23(76.7%)patients in the combined treatment group and 20(71.4%)in the control group achieved CR;two patients in the control group achieved CR after converting to the combined treatment.The recurrence rate did not differ significantly between the control group and combined treatment group(30.0%vs 22.7%,P>0.05).Ten(35.7%)patients in the control group experienced significant weight gain of 5.7±6.1 kg,while none of the patients receiving the combined treatment exhibited significant body weight changes.Compared with the control group,the patients receiving the combined treatment showed enhanced endometrial expressions of IGFBP-rP1 and p-AMPK with lowered p-Akt expression.Conclusion Metformin combined with MA may provide an effective option for fertility-sparing treatment of AEH and grade 1 stage IA EAC,and the clinical benefits of metformin for controlling MA-induced weight gain and promoting endometrial expressions of IGFBP-rP1 and p-AMPK while inhibiting p-Akt expression warrants further study. 展开更多
关键词 endormetrial adenocarcinoma METFORMIN atypical endometrial hyperplasia fertility-sparing treatment megestrol acetate insulin-like growth factor binding protein-related protein 1
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ZNF554 Inhibits Endometrial Cancer Progression via Regulating RBM5 and Inactivating WNT/β-Catenin Signaling Pathway
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作者 Cheng-cheng ZHU Heng-liang SUN +3 位作者 Teng-fei LONG Yuan-yuan LYU Jiang-li LIU Guan-tai NI 《Current Medical Science》 SCIE CAS 2024年第2期406-418,共13页
Objective:Uterine corpus endometrial carcinoma(UCEC),a kind of gynecologic malignancy,poses a significant risk to women’s health.The precise mechanism underlying the development of UCEC remains elusive.Zinc finger pr... Objective:Uterine corpus endometrial carcinoma(UCEC),a kind of gynecologic malignancy,poses a significant risk to women’s health.The precise mechanism underlying the development of UCEC remains elusive.Zinc finger protein 554(ZNF554),a member of the Krüppel-associated box domain zinc finger protein superfamily,was reported to be dysregulated in various illnesses,including malignant tumors.This study aimed to examine the involvement of ZNF554 in the development of UCEC.Methods:The expression of ZNF554 in UCEC tissues and cell lines were examined by qRT-PCR and Western blot assay.Cells with stably overexpressed or knocked-down ZNF554 were established through lentivirus infection.CCK-8,wound healing,and Transwell invasion assays were employed to assess cell proliferation,migration,and invasion.Propidium iodide(PI)staining combined with fluorescence-activated cell sorting(FACS)flow cytometer was utilized to detect cell cycle distribution.qRT-PCR and Western blotting were conducted to examine relative mRNA and protein levels.Chromatin immunoprecipitation assay and luciferase reporter assay were used to explore the regulatory role of ZNF554 in RNA binding motif 5(RBM5).Results:The expression of ZNF554 was found to be reduced in both UCEC samples and cell lines.Decreased expression of ZNF554 was associated with higher tumor stage,decreased overall survival,and reduced disease-free survival in UCEC.ZNF554 overexpression suppressed cell proliferation,migration,and invasion,while also inducing cell cycle arrest.In contrast,a decrease in ZNF554 expression resulted in the opposite effect.Mechanistically,ZNF554 transcriptionally regulated RBM5,leading to the deactivation of the Wingless(WNT)/β-catenin signaling pathway.Moreover,the findings from rescue studies demonstrated that the inhibition of RBM5 negated the impact of ZNF554 overexpression onβ-catenin and p-glycogen synthase kinase-3β(p-GSK-3β).Similarly,the deliberate activation of RBM5 reduced the increase inβ-catenin and p-GSK-3βcaused by the suppression of ZNF554.In vitro experiments showed that ZNF554 overexpression-induced decreases in cell proliferation and migration were counteracted by RBM5 knockdown.Additionally,when RBM5 was overexpressed,it hindered the improvements in cell proliferation and migration caused by reducing the ZNF554 levels.Conclusion:ZNF554 functions as a tumor suppressor in UCEC.Furthermore,ZNF554 regulates UCEC progression through the RBM5/WNT/β-catenin signaling pathway.ZNF554 shows a promise as both a prognostic biomarker and a therapeutic target for UCEC. 展开更多
关键词 zinc finger protein 554 endometrial carcinoma RNA binding motif 5 Wingless/β-catenin signaling pathway
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Crosslink among cyclin-dependent kinase 9,ATP binding cassette transporter G2 and Beclin 1 in colorectal cancer
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作者 Zhong-Bao Shao Ke He +1 位作者 Yu-Bin Su Zhi Shi 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第12期4778-4781,共4页
Colorectal cancer(CRC)ranks third in the number of cancers mainly because of the inability to diagnose it at an early stage.The pathogenesis of CRC is complicated,which is the result of the complex interaction of mult... Colorectal cancer(CRC)ranks third in the number of cancers mainly because of the inability to diagnose it at an early stage.The pathogenesis of CRC is complicated,which is the result of the complex interaction of multiple genetic and environmental factors.Currently,one of the main treatments for CRC is chemotherapy.But the primary cause of CRC treatment failure is drug resistance.The expression of cyclin-dependent kinase 9(CDK9)was correlated with elevated autophagy levels in colon cancer,and high expression of CDK9 indicates a poor prognosis in CRC.The incidence of autophagy and the expressions of Beclin 1 and ATP binding cassette transporter G2 are different in left and right colon cancer,and autophagy may be involved in the occurrence of chemotherapy resistance.In this article,the roles of CDK9,ATP binding cassette transporter G2 and Beclin 1 in CRC were elucidated,emphasizing the linkages among them and providing potential therapeutic targets of CRC. 展开更多
关键词 Cyclin-dependent kinase 9 ATP binding cassette transporter G2 Beclin 1 Colorectal cancer CHEMOTHERAPY
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N6-methyladenosine methylation regulates the tumor microenvironment of Epstein-Barr virus-associated gastric cancer
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作者 Yu Zhang Fang Zhou +7 位作者 Ming-Yu Zhang Li-Na Feng Jia-Lun Guan Ruo-Nan Dong Yu-Jie Huang Su-Hong Xia Jia-Zhi Liao Kai Zhao 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第6期2555-2570,共16页
BACKGROUND N6-methyladenosine(m6A)methylation modification exists in Epstein-Barr virus(EBV)primary infection,latency,and lytic reactivation.It also modifies EBV latent genes and lytic genes.EBV-associated gastric can... BACKGROUND N6-methyladenosine(m6A)methylation modification exists in Epstein-Barr virus(EBV)primary infection,latency,and lytic reactivation.It also modifies EBV latent genes and lytic genes.EBV-associated gastric cancer(EBVaGC)is a distinctive molecular subtype of GC.We hypothesized EBV and m6A methylation regulators interact with each other in EBVaGC to differentiate it from other types of GC.AIM To investigate the mechanisms of m6A methylation regulators in EBVaGC to determine the differentiating factors from other types of GC.METHODS First,The Cancer Gene Atlas and Gene Expression Omnibus databases were used to analyze the expression pattern of m6A methylation regulators between EBVaGC and EBV-negative GC(EBVnGC).Second,we identified Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)functional enrichment of m6A-related differentially expressed genes.We quantified the relative abundance of immune cells and inflammatory factors in the tumor microenvironment(TME).Finally,cell counting kit-8 cell proliferation test,transwell test,and flow cytometry were used to verify the effect of insulin-like growth factor binding protein 1(IGFBP1)in EBVaGC cell lines.RESULTS m6A methylation regulators were involved in the occurrence and development of EBVaGC.Compared with EBVnGC,the expression levels of m6A methylation regulators Wilms tumor 1-associated protein,RNA binding motif protein 15B,CBL proto-oncogene like 1,leucine rich pentatricopeptide repeat containing,heterogeneous nuclear ribonucleoprotein A2B1,IGFBP1,and insulin-like growth factor 2 binding protein 1 were significantly downregulated in EBVaGC(P<0.05).The overall survival rate of EBVaGC patients with a lower expression level of IGFBP1 was significantly higher(P=0.046).GO and KEGG functional enrichment analyses showed that the immunity pathways were significantly activated and rich in immune cell infiltration in EBVaGC.Compared with EBVnGC,the infiltration of activated CD4+T cells,activated CD8+T cells,monocytes,activated dendritic cells,and plasmacytoid dendritic cells were significantly upregulated in EBVaGC(P<0.001).In EBVaGC,the expression level of proinflammatory factors interleukin(IL)-17,IL-21,and interferon-γ and immunosuppressive factor IL-10 were significantly increased(P<0.05).In vitro experiments demonstrated that the expression level of IGFBP1 was significantly lower in an EBVaGC cell line(SNU719)than in an EBVnGC cell line(AGS)(P<0.05).IGFBP1 overexpression significantly attenuated proliferation and migration and promoted the apoptosis levels in SNU719.Interfering IGFBP1 significantly promoted proliferation and migration and attenuated the apoptosis levels in AGS.CONCLUSION m6A regulators could remodel the TME of EBVaGC,which is classified as an immune-inflamed phenotype and referred to as a“hot”tumor.Among these regulators,we demonstrated that IGFBP1 affected proliferation,migration,and apoptosis. 展开更多
关键词 N6-methyladenosine methylation Tumor microenvironment Epstein-Barr virus Gastric cancer Insulin-like growth factor binding protein 1
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Evaluating new biomarkers for diabetic nephropathy:Role ofα2-macroglobulin,podocalyxin,α-L-fucosidase,retinol-binding protein-4,and cystatin C
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作者 Jing-Jing Li Ru-La Sa +1 位作者 Yu Zhang Zhao-Li Yan 《World Journal of Diabetes》 SCIE 2024年第6期1212-1225,共14页
BACKGROUND The intricate relationship between type 2 diabetes mellitus(T2DM)and diabetic nephropathy(DN)presents a challenge in understanding the significance of various biomarkers in diagnosis.AIM To elucidate the ro... BACKGROUND The intricate relationship between type 2 diabetes mellitus(T2DM)and diabetic nephropathy(DN)presents a challenge in understanding the significance of various biomarkers in diagnosis.AIM To elucidate the roles and diagnostic values ofα2-macroglobulin(α2-MG),podocalyxin(PCX),α-L-fucosidase(AFU),retinol-binding protein-4(RBP-4),and cystatin C(CysC)in DN.METHODS From December 2018 to December 2020,203 T2DM patients were enrolled in the study.Of these,115 were diagnosed with DN(115 patients),while the remaining 88 patients were classified as non-DN.The urinary levels ofα2-MG,PCX,and AFU and the serum concentrations RBP-4 and CysC were measured in conjunction with other relevant clinical indicators to evaluate their potential correlations and diagnostic utility.RESULTS After adjustments for age and gender,significant positive correlations were observed between the biomarkers CysC,RBP-4,α2-MG/urinary creatinine(UCr),PCX/UCr,and AFU/UCr,and clinical indicators such as urinary albumin-to-creatinine ratio(UACR),serum creatinine,urea,24-h total urine protein,and neutrophil-to-lymphocyte ratio(NLR).Conversely,these biomarkers exhibited negative correlations with the estimated glomerular filtration rate(P<0.05).Receiver operating characteristic(ROC)curve analysis further demonstrated the diagnostic performance of these biomarkers,with UACR showcasing the highest area under the ROC curve(AUC^(ROC))at 0.97.CONCLUSION This study underscores the diagnostic significance ofα2-MG,PCX,and AFU in the development of DN.The biomarkers RBP-4,CysC,PCX,AFU,andα2-MG provide promising diagnostic insights,while UACR is the most potent diagnostic biomarker in assessing DN. 展开更多
关键词 Α2-MACROGLOBULIN Podocalysin Α-L-FUCOSIDASE Retinol binding protein-4 Cystatin C Diabetic nephropathy
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Exosomes derived from microglia overexpressing miR-124-3p alleviate neuronal endoplasmic reticulum stress damage after repetitive mild traumatic brain injury
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作者 Yan Wang Dai Li +12 位作者 Lan Zhang Zhenyu Yin Zhaoli Han Xintong Ge Meimei Li Jing Zhao Shishuang Zhang Yan Zuo Xiangyang Xiong Han Gao Qiang Liu Fanglian Chen Ping Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2010-2018,共9页
We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repet... We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repetitive mild traumatic brain injury remains unclear.In this study,we first used an HT22 scratch injury model to mimic traumatic brain injury,then co-cultured the HT22 cells with BV2 microglia expressing high levels of miR-124-3p.We found that exosomes containing high levels of miR-124-3p attenuated apoptosis and endoplasmic reticulum stress.Furthermore,luciferase reporter assay analysis confirmed that miR-124-3p bound specifically to the endoplasmic reticulum stress-related protein IRE1α,while an IRE1αfunctional salvage experiment confirmed that miR-124-3p targeted IRE1αand reduced its expression,thereby inhibiting endoplasmic reticulum stress in injured neurons.Finally,we delivered microglia-derived exosomes containing miR-124-3p intranasally to a mouse model of repetitive mild traumatic brain injury and found that endoplasmic reticulum stress and apoptosis levels in hippocampal neurons were significantly reduced.These findings suggest that,after repetitive mild traumatic brain injury,miR-124-3 can be transferred from microglia-derived exosomes to injured neurons,where it exerts a neuroprotective effect by inhibiting endoplasmic reticulum stress.Therefore,microglia-derived exosomes containing miR-124-3p may represent a novel therapeutic strategy for repetitive mild traumatic brain injury. 展开更多
关键词 apoptosis C/EBP homologous protein endoplasmic reticulum stress EXOSOME inositol-requiring enzyme MICROGLIA miR-124-3p neuron repetitive mild traumatic brain injury X-box binding protein 1
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GATA binding protein 2 mediated ankyrin repeat domain containing 26 high expression in myeloid-derived cell lines
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作者 Yang-Zhou Jiang Lan-Yue Hu +11 位作者 Mao-Shan Chen Xiao-Jie Wang Cheng-Ning Tan Pei-Pei Xue Teng Yu Xiao-Yan He Li-Xin Xiang Yan-Ni Xiao Xiao-Liang Li Qian Ran Zhong-Jun Li Li Chen 《World Journal of Stem Cells》 SCIE 2024年第5期538-550,共13页
BACKGROUND Thrombocytopenia 2,an autosomal dominant inherited disease characterized by moderate thrombocytopenia,predisposition to myeloid malignancies and normal platelet size and function,can be caused by 5’-untran... BACKGROUND Thrombocytopenia 2,an autosomal dominant inherited disease characterized by moderate thrombocytopenia,predisposition to myeloid malignancies and normal platelet size and function,can be caused by 5’-untranslated region(UTR)point mutations in ankyrin repeat domain containing 26(ANKRD26).Runt related transcription factor 1(RUNX1)and friend leukemia integration 1(FLI1)have been identified as negative regulators of ANKRD26.However,the positive regulators of ANKRD26 are still unknown.AIM To prove the positive regulatory effect of GATA binding protein 2(GATA2)on ANKRD26 transcription.METHODS Human induced pluripotent stem cells derived from bone marrow(hiPSC-BM)INTRODUCTION Ankyrin repeat domain containing protein 26(ANKRD26)acts as a regulator of adipogenesis and is involved in the regulation of feeding behavior[1-3].The ANKRD26 gene is located on chromosome 10 and shares regions of homology with the primate-specific gene family POTE.According to the Human Protein Atlas database,the ANKRD26 protein is localized to the Golgi apparatus and vesicles,and its expression can be detected in nearly all human tissues[4].Moreover,UniProt annotation revealed that ANKRD26 is localized in the centrosome and contains coiled-coil domains formed by spectrin helices and ankyrin repeats[5,6].The most common disease related to ANKRD26 is thrombocytopenia 2(THC2),which is a rare autosomal dominant inherited disease characterized by lifelong mild-to-moderate thrombocytopenia and mild bleeding[7-9].Caused by the variants in the 5’-untranslated region(UTR)of ANKRD26,THC2 is defined by a decrease in the number of platelets in circulating blood and results in increased bleeding and decreased clotting ability[8,10].Due to the point mutations that occur in the 5’-UTR of ANKRD26,its negative transcription factors(TFs),Runt related transcription factor 1(RUNX1)and friend leukemia integration 1(FLI1),lose their repression effect[11].The persistent expression of ANKRD26 increases the activity of the mitogen activated protein kinase and extracellular signal regulated kinase 1/2 signaling pathways,which are potentially involved in the regulation of thrombopoietin-dependent signaling and further impair proplatelet formation by megakaryocytes(MKs)[11].However,the positive regulators of ANKRD26,which might be associated with THC2 pathology,are still unknown. 展开更多
关键词 Ankyrin repeat domain containing 26 GATA binding protein 2 Thrombocytopenia 2 Transcriptional regulation Myeloid-derived cell lines
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Identification of immune feature genes and intercellular profiles in diabetic cardiomyopathy
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作者 Ze-Qun Zheng Di-Hui Cai Yong-Fei Song 《World Journal of Diabetes》 SCIE 2024年第10期2093-2110,共18页
BACKGROUND Diabetic cardiomyopathy(DCM)is a multifaceted cardiovascular disorder in which immune dysregulation plays a pivotal role.The immunological molecular mechanisms underlying DCM are poorly understood.AIM To ex... BACKGROUND Diabetic cardiomyopathy(DCM)is a multifaceted cardiovascular disorder in which immune dysregulation plays a pivotal role.The immunological molecular mechanisms underlying DCM are poorly understood.AIM To examine the immunological molecular mechanisms of DCM and construct diagnostic and prognostic models of DCM based on immune feature genes(IFGs).METHODS Weighted gene co-expression network analysis along with machine learning methods were employed to pinpoint IFGs within bulk RNA sequencing(RNA-seq)datasets.Single-sample gene set enrichment analysis(ssGSEA)facilitated the analysis of immune cell infiltration.Diagnostic and prognostic models for these IFGs were developed and assessed in a validation cohort.Gene expression in the DCM cell model was confirmed through real time-quantitative polymerase chain reaction and western blotting techniques.Additionally,single-cell RNA-seq data provided deeper insights into cellular profiles and interactions.RESULTS The overlap between 69 differentially expressed genes in the DCM-associated module and 2483 immune genes yielded 7 differentially expressed immune-related genes.Four IFGs showed good diagnostic and prognostic values in the validation cohort:Proenkephalin(Penk)and retinol binding protein 7(Rbp7),which were highly expressed,and glucagon receptor and inhibin subunit alpha,which were expressed at low levels in DCM patients(all area under the curves>0.9).SsGSEA revealed that IFG-related immune cell infiltration primarily involved type 2 T helper cells.High expression of Penk(P<0.0001)and Rbp7(P=0.001)was detected in cardiomyocytes and interstitial cells and further confirmed in a DCM cell model in vitro.Intercellular events and communication analysis revealed abnormal cellular phenotype transformation and signaling communication in DCM,especially between mesenchymal cells and macrophages.CONCLUSION The present study identified Penk and Rbp7 as potential DCM biomarkers,and aberrant mesenchymal-immune cell phenotype communication may be an important aspect of DCM pathogenesis. 展开更多
关键词 Diabetic cardiomyopathy Immune feature genes PROENKEPHALIN Retinol binding protein 7 Immune cell infiltration Intercellular communication
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